Podcasts about royalties

I've been a full-time creator for 8 years now and have earned $2,192,000 since 2022. I've spent a LOT of time and money experimenting with different ways to make money on the internet, so I'm going to rank them. The best and the worst. I show you 15 different revenue streams and rate them from S to F based on their potential versus the effort required. By the very end of the video, you'll know which ones are right for you. And at any point, if you agree or disagree, let me know in the comments. ⁠⁠⁠⁠⁠⁠⁠Full transcript and show notes⁠⁠⁠⁠⁠⁠⁠ *** TIMESTAMPS (00:32) AdSense (01:36) Sponsorship & Brand Deals (03:30) Content Memberships (04:30) Done-For-You Services (05:27) Royalties (06:28) 1-to-1 Coaching & Consulting (07:38) Affiliates (09:36) User Generated Content (UGC) (10:17) Group Programs (11:25) Digital Products (12:56) Speaking (14:27) Live Events (15:53) Community Memberships *** RECOMMENDED NEXT EPISODE → ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠#267: When to use low-ticket offers, refund policies, how much I earned in the last 12 months, and my 5-year vision [Ask CS Pt. 1] *** ASK CREATOR SCIENCE → ⁠⁠⁠⁠⁠⁠⁠Submit your question here⁠⁠⁠⁠⁠⁠⁠ *** WHEN YOU'RE READY

In this JCO Article Insights episode, Dr. Ece Cal interviews Dr. Martin Wermke, author of the JCO article, "Phase I Dose-Escalation Results for the Delta-Like Ligand 3/CD3 IgG-Like T-Cell Engager Obrixtamig (BI 764532) in Patients With Delta-Like Ligand 3+ Small Cell Lung Cancer or Neuroendocrine Carcinomas." TRANSCRIPT The disclosures for guests on this podcast can be found in the transcript. Dr. Ece Cali: Welcome to this episode of JCO Article Insights. This is Dr. Ece Cali, JCO editorial fellow, and today I am joined by Dr. Martin Wermke, Professor for Experimental Cancer Therapy at Dresden University of Technology, to discuss the manuscript “Phase 1 Dose-Escalation Results for the Delta-Like Ligand 3/CD3 IgG-like T-Cell Engager Obrixtamig in Patients with DLL3+ Small Cell Lung Cancer or Neuroendocrine Carcinomas.” Obrixtamig is a bispecific T-cell engager that binds to DLL3 on tumor cells and CD3 on T-cells. This manuscript presents the phase 1A dose escalation results of Obrixtamig in patients with DLL3+ small cell lung cancer and neuroendocrine carcinomas. In this study, 168 patients were treated with Obrixtamig across four different dosing regimens. 49% of the patients had small cell lung cancer, 42% had extrapulmonary neuroendocrine carcinoma, and 8% had large cell neuroendocrine carcinoma of the lung. Patients received a median of two prior lines of therapy. 33% of the patients had brain metastases at baseline. Of note, this trial did not mandate baseline brain imaging. Maximum tolerated dose was not reached. 88% of the patients experienced a treatment-related adverse event, however, only 3.6% of the patients had to discontinue treatment due to treatment-related AEs, and dose reduction due to treatment-related AEs was documented in 2.4% of the patient population. Similar to the other DLL3-targeted bi-therapies, the most common adverse events included CRS in 57%, dysgeusia in 23%, and pyrexia in 21% of the patients. CRS events were mostly mild. They occurred more frequently in the first two to three doses. 9% of the patients experienced ICANS, of which 3% were graded as Grade 3 or higher. And let's review the efficacy results. Responses were only seen in patients who received 90 microgram per kg or more once weekly or once every three weeks dosing. The objective response rate in patients who received an effective dose was 28%. If we review by tumor type, 21% of the small cell lung cancer patients, 27% of the extrapulmonary neuroendocrine carcinoma patients, and 70% of the large cell neuroendocrine carcinoma patients had objective response. Median duration of response was 8.5 months, though this data is immature due to short follow-up. Dr. Wermke, DLL3-targeted bispecific T-cell engagers are reshaping the treatment landscape of small cell lung cancer. This trial investigates Obrixtamig in other high-grade neuroendocrine tumors as well. Can you put this trial into context for us and explain why it may represent an important step forward? Dr. Martin Wermke: Yeah, thank you for providing me with the opportunity to discuss our data today. I think the data with Obrixtamig in small cell lung cancer are largely similar to what has been observed with other bispecific T-cell engagers such as tarlatamab with respect to the response rate and duration. It has, however, been to be mentioned that BI 1438001 had a bit more liberal inclusion criteria than other trials around. You already mentioned the fact that we allowed the inclusion of patients without mandatory brain imaging, which led to some patients having their brain mets been diagnosed during the treatment with obrixtamig and then adding to the progressive disease patients. That is something which was not the case with the tarlatamab trials where you really had to have a brain imaging before, and in the Phase 1 trial you were even required to treat the brain mets before you included the patient. So it is a bit different, more poorest patient population. I think the trial adds on existing data by being the first trial to also include non-SCLC neuroendocrine carcinoma of other origin, for example from the gastrointestinal tract, and also by including large cell neuroendocrine carcinoma of the lung, which is a really hard to treat pulmonary neoplasm which currently lacks any standardized treatment. So that is really a step forward which we will build on in the future. Dr. Ece Cali: And one thing I would note in this trial, only patients with tumor expressing DLL3 were enrolled. Can you tell us a little bit more about this target, DLL3 in the context of neuroendocrine tumors, and does DLL3 expression predict clinical outcomes after treatment with DLL3 BiTEs, or do we actually need other predictive biomarkers for these novel agents? Dr. Martin Wermke: Yeah, thank you. That's a pretty interesting question. First of all, DLL3 is an atypical notch ligand, which is expressed by the majority of neuroendocrine carcinomas, virtually absent on healthy adult tissues. Therefore, turning it really into a bona fide target for T-cell engaging therapies, pretty low risk for on-target off-tumor side effects. We found that in all the patients we screened, we had an expression rate of about 94% in small cell lung cancer, 80% of large cell neuroendocrine carcinoma of the lung were positive, and also about 80% of the extrapulmonary neuroendocrine carcinoma. So it's really a high prevalence. So the fact that we only included DLL3+ tumors still means we included most of the patients that presented with these diseases. I think at the moment there are no data suggesting a clear-cut association between DLL3 expression levels and outcome on DLL3 CD3 T-cell engagers. There's also not a lot published. If you want to find this out for tarlatamab, you have to look into their patent to really see the data, but it's not clear-cut and I'm sure we need other markers to complement that. And I think what probably plays a major role is intrinsic T-cell fitness. So the question how really diseased your T-cells are, how old you are, because age also correlates with the fitness of the immune system, and other patient characteristics such as tumor burden, we've seen all across the board that the higher the tumor burden, the lower the rate of prolonged response is in such trials. And I also think we need to focus on other components of the tumor microenvironment. So see how high the T-cell infiltration with obrixtamig is and how abundant suppressive elements like regulatory T-cells or myeloid-derived suppressive cells are. That is work which is currently being done. Data are emerging, but I don't think that at the moment we have any clear biomarker helping us to select who should not receive DLL3 T-cell engagers. Dr. Ece Cali: Those are great points and there is a lot we need to learn about how to use these novel agents in the future. I'd like to highlight the results in large cell neuroendocrine carcinoma of the lung. The response rate in this group was remarkably high at 70%. Though we should note the small sample size of only 14 patients in this trial. After first line chemoimmunotherapy, current approved options for this population have very modest clinical activity. Given these trial results, how do you envision the field moving forward for patients with large cell neuroendocrine carcinoma? Dr. Martin Wermke: Yeah, I think LCNEC is really an area which urgently needs further improvement of therapeutic standards. At the moment, as I said, there is no real standard. We are usually extrapolating from results we have in small cell lung cancer or non-small cell lung cancer, but I don't think we have too many prospective trials really informing this. Of course, 14 patients is a small sample size, but I think it's still fair to say that we can claim that DLL3 T-cell engagers are not doing worse in LCNEC than they do in SCLC. And that's why I think we really need to move forward clinical trials that are specifically targeting this population. Although I fear a bit that, given the rareness of this disease and the aggressiveness of its phenotype, that this is probably not the main focus of the pharmaceutical industry. So I think it's up to us academic investigators to really come up with investigator-initiated trials trying to fill the knowledge gaps we have here. Dr. Ece Cali: And one more thing that I want to talk about is the accessibility for these drugs. These novel agents are showing real promise in improving outcomes for patients with high-grade neuroendocrine tumors, an area where progress has been limited until very recently. However, as DLL3 BiTEs become more widely used, issues of logistics and access come into sharper focus. With unique toxicities and the specialized monitoring, their use is restricted to certain centers. Looking ahead, what kinds of strategies could help mitigate some of these adverse events or make these treatments more broadly available? Dr. Martin Wermke: Yeah, I think if you look at countries like the United States where tarlatamab has already been approved, we can see how the management strategies are evolving. I've heard about a colleague equipping their patients with thermometers and a pill of Dexamethasone, alongside with a temperature control protocol and clearly instructing them, "If you measure a temperature above a certain level then start taking the Dexamethasone and come back to our office and we're going to take care of you." I think that's one way to move forward. I think we are lucky in a way that CRS usually manifests within the first 24 hours. This was the same in our study, like in the tarlatamab studies. So we really know when the time of trouble is for our patients. And in this time, I think we need to instruct the patients to stay close to the hospital. I don't think we need to hospitalize all of them, but we probably need them to stay in a nearby hotel to be able to reach the emergency room if needed in a short period of time. And I think we can also learn in this strategy how to manage bispecific antibodies from the experience our colleagues in hematology had because they have been using bispecific T-cell engagers for quite some years right now and they developed strategies and networks that were able to successfully treat these patients also on an outpatient basis. And I think that is clearly an experience we need to follow, acknowledging that we are talking about diseases which are much more frequent than the standard hematology indications. Dr. Ece Cali: Thank you so much, Dr. Wermke, for this informative discussion and for sharing your perspective on this evolving field. Dr. Martin Wermke: Yeah, thank you for providing me with the opportunity to talk about data. It was really great being able to share that, and I really think that we are just at the beginning of a new exciting area for the treatment of neuroendocrine carcinomas, and I think much improvement is yet to come for our patients. Dr. Ece Cali: Yes, that's really exciting. And thank you everyone for listening to JCO Article Insights. Please come back for more interviews and article summaries and be sure to leave us a rating and review so others can find our show. For more podcasts and episodes from ASCO, please visit asco.org/podcasts. The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on this podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement. Dr. Martin Wermke's Disclosures Honoraria: Lilly, Boehringer Ingelheim, SYNLAB, Janssen, Merck Serono, GWT, Amgen, Novartis, Pfizer,  BMS GmbH & Co. KG, Regeneron, MJH/PER, Takeda Consulting or Advisory Role: Bristol-Myers Squib, Novartis, Lilly, Boehringer Ingelheim, ISA Pharmaceuticals, Amgen, immatics, Bayer, ImCheck therapeutics, AstraZeneca, Tacalyx, Regeneron, Daiichi Sankyo Europe GmbH, Zymeworks, PharmaMar, Iovance Biotherapeutics, T-Knife, Genentech Research Funding: Roche Patents, Royalties, Other Intellectual Property Travel, Accommodations, Expenses: Pfizer, Bristol-Myers Squibb, AstraZeneca,  Amgen,  GEMoaB, Sanofi/Aventis, immatics,  Merck Serono, Janssen Oncology, Iovance Biotherapeutics, Daiichi Sankyo Europe GmbH"

Dan O'Flaherty, CEO of Versamet Royalties (TSX.V: VMET), joins me to provide an update on the recent acquisition of both a silver stream and net smelter royalty on cash-flowing producing assets from Appian Capital.  We also take a deeper dive into the value proposition embedded in their portfolio of streams and royalties, and the triple-pronged approach to growth for this newer royalty company, that just listed publicly back in May of this year. Dan previously led Maverix Metals, which sold to Triple Flag in 2023, and now he's building Versamet to fill the gap between junior royalty players and the multi‑billion‑dollar majors.   Key Highlights from Our Discussion:   Closed an agreement on September 24th for the acquisition of two long-life, high-quality, producing assets from Appian Capital Advisory; with immediate cash flow for an up-front cash consideration of $125 million. Rosh Pinah Zinc - a 90% silver stream an operating underground mine in Namibia with over 55 years of mining history and a long history of resource additions and significant exploration potential Santa Rita - a 2.75% net smelter return royalty (NSR) on a top tier nickel sulphide mine located in Bahia state, Brazil, currently producing from an open pit. The Stream and NSR Royalty are expected to contribute approximately 5,000 gold equivalent ounces ("GEOs") in 2026 using analyst consensus metal prices. Cash‑flow focus: From ~10,000 GEOs in 2025 to ~20,000 GEOs by 2026, translating to over $70M in annual revenue targeted for next year, using consensus gold prices, and even higher than that at current spot prices. Balance sheet strength: Paid off initial debt out of robust revenues, before adding this recent debt on the back of these 2 acquisitions; with a roadmap to paying that back down in an accelerated fashion from quarterly cashflows. Rapid portfolio growth: Over US$400M in acquisitions since 2022, growing Versamet's market cap to over CAD$800 million. We review how several key strategic stakeholders got into partnership with Versamet including: B2Gold (33%), Sandstorm (25%), and Equinox Gold (13%) as cornerstone shareholders, providing technical strength and deal flow. Investors today can get an early mover advantage before more institutional investors and passive fund investments have entered the story. Triple-pronged approach to growth: (1) Near‑term organic growth from within their existing portfolio of royalties and streams, (2) future accretive acquisitions, and (3) the coming U.S. listing for more liquidity, a broader investor base, and the potential inclusion in funds and ETFs.     If you have any questions for Dan regarding Versamet Royalties, then please email those in to me at Shad@kereport.com.   Click here to follow the latest news from Versamet Royalties

Fred Bell, CEO of Elemental Altus Royalties (TSX.V:ELE) (OTCQX:ELEMF), and Dave Cole, CEO of EMX Royalty Corp (NYSE American: EMX) (TSXV: EMX), both join me to unpack the key transaction details, synergies, and growth profile emerging from the business combination of both companies into the emerging Elemental Royalty Corp.  In the new combined entity, Dave will be the CEO, and Fred will be the President and COO, with the balance of the management team and board being a solid blend of the 2 companies current teams.   Dave starts us off with the big-picture rationale for this merger, creating a larger royalty company of scale, graduating up to the mid-tier category, with more analyst coverage and liquidity, a better cost of capital, the financial strength from the backing of the key strategic shareholder Tether Investments, and the potential to rerate in the future to a better price to net asset value multiple more in alignment with larger royalty peers.   Fred then takes us through the transaction specifics of the merger, including the recent financing, share roll back, and US big board exchange listing that were all announced earlier this month, in concert with this business combination. Fred also outlines the importance of having Tether Investments as their key strategic shareholder, and they financially backstop the kinds of accretive acquisitions that they can now go after. He also explains why they made the choice to establish an institutional account to gain exposure to Tether Gold (XAUt), a tokenized asset backed 1:1 by physical gold, to diversify the Company's treasury and increase exposure to rising gold prices with enhanced liquidity and efficiency.   We also dive into updates on their key cornerstone royalty partner projects: Timok, Laverton, Karlawinda, and Caserones. the organic development growth still on tap in their portfolio of royalties, the future upside of the continued royalty generation strategy, and a look ahead to future larger acquisitions than were possible for both companies up until the creation of this new combined vehicle.   If you have any follow up questions for Dave or Fred regarding the merger of Elemental Altus Royalties with EMX Royalty, into the new Elemental Royalty Corp, then please email them to me at Shad@kereport.com.   In full disclosure, Shad is a shareholder of both Elemental Altus Royalties and EMX Royalty Corp at the time of this recording, and may choose to buy or sell shares at any time.   Click here to learn more about the Elemental Altus and EMX Royalty merger   Click here to view recent news on Elemental Altus Royalties   Click here to view recent news on EMX Royalty

Every masterpiece you've ever consumed likely passed through a licensing agreement first. That catchy song in your favorite commercial? Licensed. The superhero logo on your coffee mug? Licensed. The technology powering your smartphone? Licensed hundreds of times over. Licensing represents the hidden architecture behind innovation empires, allowing creators to extend their reach without surrendering control. Unlike selling your intellectual property outright, licensing lets you maintain ownership while granting permission for others to use it under specific conditions – essentially renting out a room while remaining the landlord.The potential of licensing spans virtually every form of intellectual property. Patents enable inventors to collect royalties from global manufacturers without running factories. Trademarks allow fashion brands and sports teams to appear on merchandise worldwide. Copyrights drive music, publishing, and streaming industries. Even carefully protected trade secrets can be licensed as valuable know-how.But successful licensing requires methodical preparation. You must clearly establish ownership, precisely define scope, protect confidentiality during negotiations, package assets for seamless transition, establish defensible royalty models, and determine governance structures. Finding the right licensees demands strategic targeting – from identifying companies in similar patent classes to exploring industry standards programs and attending specialized trade shows.The negotiation process benefits from structured frameworks: separating positions from interests, understanding your alternatives, presenting multiple equivalent offers, and stress-testing deals through financial modeling. Equally important is recognizing red flags: licensees who overpromise, resist transparency, fight performance standards, demand excessive exclusivity, or operate in challenging regulatory environments.Remember that licenses exist in dynamic markets with changing conditions. Know when to renegotiate (when fundamental assumptions shift), when to walk away (when partners consistently underperform), and when litigation becomes necessary (when your rights are genuinely threatened).Want to develop your own IP protection strategy? Check out "Protection for the Inventive Mind" – available now on Amazon in print and Kindle formats.Get the book!Send us a textSupport the show

In this episode, we unpack the insights from the recent IPSeries webinar exploring the evolving landscape of Collective Management Organizations (CMOs) across Africa and the globe. From the challenges of royalty collection and distribution to the legal frameworks shaping copyright enforcement, we dive into a comparative review of global versus local approaches to rights management.Experts from across the creative and legal sectors weigh in on:The role of CMOs in empowering artists and creatorsStructural and policy differences between African CMOs and their global counterpartsThe impact of digital platforms and cross-border licensingStrategies for improving transparency, accountability, and efficiencyWhether you're a creator, legal professional, or policy enthusiast, this episode offers a compelling look at how collective rights management is transforming and what it means for the future of intellectual property in Africa and beyond.So grab your headphones, settle in, and let’s explore how collective rights management is reshaping the future of intellectual property on the continent and beyond.Please leave your thoughts and opinions by commenting via email at ipseriesinfo@gmail.com or by tweeting us at @ipseries1. And don't forget to subscribe to my podcast for more intellectual property (IP) insights and analysis.Thank you for listening, and see you next time on the IP Series podcast!IPSERIES PODCAST- Facebook: https://web.facebook.com/groups/836484013662125/- Instagram: ⁠Instagram⁠- Email: ipseriesinfo@gmail.com=================================SOCIAL MEDIA BY: Rita Anwiri Chindah=================================LOGO DESIGN BY: Rita Anwiri Chindah ⁠ipseries_with_reedah | Twitter, Instagram, Facebook | https://linktr.ee/ipseries_with_reedah?subscribe

Dr. Monty Pal and Dr. Mina Sedrak discuss the science behind cancer treatment-induced accelerated aging and the development of drug therapies and technologies aimed at helping older patients and cancer survivors. TRANSCRIPT Transcript: Cancer and Aging: Researching the Path to Longer, More Vibrant Lives Dr. Monty Pal: Hello, and welcome to the ASCO Daily News Podcast. I am Dr. Monty Pal. I am a medical oncologist and professor and vice chair of medical oncology here at the City of Hope Comprehensive Cancer Center. I am also host of this podcast. Today, we are going to be talking to somebody that I consider to be my little brother, if you will, in oncology, Mina Sedrak. Mina is an expert in the area of cancer and aging, which really includes the development of drug therapies and technologies that help enable older adults and survivors to live longer, healthier, and more vibrant lives. I am really excited to chat with him. He is an expert not just in cancer and aging but also breast cancer. He was my former colleague here at City of Hope before he moved over to the UCLA Jonsson Comprehensive Cancer Center, where he is an associate professor and director there of the Cancer and Aging Program. Dr. Sedrak's research involves mechanisms behind cancer treatment-induced accelerated aging and really aims to take this science into more of a therapeutic direction, which I am super, super excited about.  Mina, thanks so much for joining us today, and just FYI for our listeners, we have all of our disclosures in the transcript of this episode. Dr. Mina Sedrak: Thank you, Monty. Thank you, Dr. Pal, for having me. I am really excited to be here. Dr. Monty Pal: I feel like we have to go on a first-name basis here with how well we know each other. So Mina, you and I together have witnessed this evolution in cancer and aging. I mean, both of us worked together here with just a legendary figure in the field of geriatric oncology, I will call it, Dr. Arti Hurria, mentor to me, mentor to you, mentor to so many. Can you give us a sense of where cancer and aging has gone since the time that you and I started here together at City of Hope? Dr. Mina Sedrak: Dr. Hurria and her collaborators, Dr. [Willliam] Dale and Dr. [Supriya] Mohile, they were like huge pioneers in the field. They were one of the very first people to highlight the importance of looking at older adults beyond just their chronological age and their comorbidities and moving us beyond just seeing patients and making decisions using what we call the eyeball test. "Oh, this person looks fit or not fit, frail or robust," to really using objective measures to assess our patient's health status and incorporate that assessment into our evaluation of the treatment, prognostication, and discussions with our patients throughout the cancer continuum. And so that is what geriatric oncology has and continues to be, and it is a huge, important part. And their work has laid the foundation to show that when we look at our patients beyond just their chronological age and we look at their functional age, and we do these objective assessments, we can gain much more deeper information to tailor the treatment for our patient that is sitting in front of us, rather than do a prescriptive treatment or over- or undertreatment in that population. So that is sort of where the field is growing, and a lot of the work now is, how do we implement that? How do we put that into clinical practice? Dr. Monty Pal: Well, let me kind of spearhead that discussion, right? I have these moments when I go to the ASCO Annual Meeting – I remember this happened to me a while ago when Dr. Jennifer Temel presented that terrific work around early palliative care interventions, right? Or it even happened to me this year, right, when Dr. Christopher Booth presented the CHALLENGE trial around exercise and colon cancer. You know, these amazing, I am going to say simple, they are not simple, but they are simple interventions relative to, you know, some of the complex drugs and mechanisms that we are using nowadays that really help outcomes for our cancer patients. The big question becomes, how do you implement, right? But my understanding is that there are easy ways for us to take tools in cancer and aging and sort of plug them into our daily practice. Am I right about that? Dr. Mina Sedrak: Yes, and that is something that they are – the Cancer and Aging Research Group, which was founded by Dr. Hurria and now is co-led by Dr. Dale, Dr. Mohile, and Dr. [Heidi] Klepin, they have been incredible at really trying to develop practical tools, like the Practical Geriatric Assessment, which is now endorsed by the ASCO and other NCCN guidelines. And so, there are tools that are becoming more and more practical to help incorporate that into clinic.  Now, what might be practical in a resource-intensive setting may not be practical in some of the limited resources, whether it is rural and/or other countries where the resources may be more limited. So that is why Cristiane Bergerot, Enrique Soto, and others have been really working hard. There was actually a really beautiful paper that was just published in the Journal of Global Oncology, where they have shown that there are guidelines [ASCO Geriatric Assessment Global Guideline] about how to implement these tests, these tools, these assessments in clinical practice, even in different resource settings. So I think we are going to get to the future where this is much more – it is definitely important, but it is much more easily ‘incorporatable' into our practice. Dr. Monty Pal: Yeah, you know how close I am to Cris, and I was so proud when I saw that paper come out. That was really exciting. You know, I skimmed it. I have to tell you, I did not get into the weeds, but it was apparent to me that, you know, some of these geriatric oncology tools are things that, you know, I could probably plug and play into my practice where I am double- and triple-booked over, you know, most slots, right? I mean, I could still probably afford a little bit of time or maybe have, like, a nurse or an extender kind of help participate in the evaluation process. I thought that was, yeah, really, really interesting. Dr. Mina Sedrak: I will just say that at UCLA, we are working with Dr. Arash Naeim, who is a geriatric oncologist, and he has developed an AI platform where the assessments can be done by an AI computer. So it is like talking to your ChatGPT. They can talk to you, and for a few minutes, they will ask you the questions. So you do not even have to fill it out on a piece of paper. You could give the patient a little iPad, put them in a private room while they are waiting for their doctor, and get the results, and it is right there for you. And so, we have been trying to think about how can technology help with the completion of the assessment, at least doing that? And I think it is actually, it has been very cool. We did a pilot study. He is writing that up, and we are going to continue to do some of this exciting work. How do we think about AI in the context of this? And, you know, older adults, they are not like what they used to be. A lot of older adults are very familiar with and comfortable with phones and computers and iPads, much more so today than they were even at the time when Dr. Hurria was alive. Dr. Monty Pal: That is so interesting. You mentioned this, the AI approach is something I have been thinking about in this context because what if, for instance, you know, we have got video monitors all over our hospital, right? What if you are actually just taking a look at that patient as they make their way towards your clinic? Capture that video, use an AI algorithm to say, "Hey, you know, the timed get-up-and-go test in this patient is not particularly good based on what I am seeing here," right? There are so many ways that you could, you know, stir the pot and come up with creative ways to get these tests done. Dr. Mina Sedrak: That's right. And Arash is looking at also sensors. So he has some studies where he is putting sensors inside people's homes, where they would put them, like, on top of an Alexa app or the equivalent. A lot of people have these apps, and basically, they can sense how you are moving around and what you are doing, just movement-wise. And then they can collect that information to gain information about your life beyond just what we are seeing in the 20-minute visit in the clinic. Even when I do a walk test where I get gait speed or physical performance, short physical performance battery, the chair sit-up, those are oftentimes a single, cross-sectional, static measure. But what about the dynamic ability of capturing what has been happening for the last 7 days? What has been happening for the last 25 days between the visits, between the cycles of chemotherapy? And could that inform how I make decisions when I see patients and who do I need to target and identify? And so, we are very excited because really at UCLA, Arash is leading the technology efforts and thinking about implementation of these important measures and these important tools but leveraging new technology. And we do not want to be behind; we want to be ahead of the game. Dr. Monty Pal: I love that idea because there is a Hawthorne effect, isn't there, where you observe a process, and it naturally gets better. I mean, when you ask that patient to get up in the clinic and move, they are probably functioning to the best of their abilities, but we could probably learn a lot from just watching how fast that patient picks up a remote control at home. Some simple movement like that that is volitional would probably help out a ton. And I got to tell you, it is so funny when you mention Arash Naeim's name. I distinctly remember him serving as an attending on the wards when he was brand new at UCLA on faculty when I was a resident there. And his dad is a legendary hematopathologist, right? Dr. Mina Sedrak: I did not know that. Dr. Monty Pal: Yeah, yeah. Faramarz Naeim wrote the book on a lot of heme-path malignancies. Incredible guy. Very, very storied hematopathologist at UCLA.  I could probably go on this topic forever, but in the interest of time, I am going to shift to something that again, I could probably talk about forever, which is this area of senescence that you are involved in. You know, you had mentioned this to me, I am going to say during your outro from City of Hope and towards your transition to UCLA, it is such an exciting area. I mean, understanding the actual biologic process of aging and using those underpinnings to really sort of tailor therapy. So tell us where the state of the science is there with this body of work that you are doing. Dr. Mina Sedrak: As I said before, we have tools now to assess patients and to then do something about the deficits. So if a patient is falling, what we do is we refer them to physical therapy where they can do fall precautions and strength training to give them the information. But all of these supportive care interventions are very important. They are great. But they oftentimes are not targeting the root cause of why they are happening. And so that is really where I have been very interested in, how can we understand why is it that something like chemotherapy or immunotherapy is causing a decline in cognitive function or a decline in physical function? And so that has really led us to think about geriatric oncology rather than a discipline of older adults, but to think about aging as a physiologic process. We are all aging. As every day goes by, we are aging. And what that means is that our bodies are accumulating damage, the cells are being exposed to various stressors, and the repair mechanisms are declining. And as we get older, it is really more damage and less repair mechanism at the cellular molecular level. And it turns out that these processes of how our cells repair and respond to damage are fundamental processes of biological aging. And there has been a large amount of preclinical and now really exciting clinical work to show that there are hallmarks that could be used to assess the rate of which we age by looking at these processes. And that includes things like epigenetics, telomeres, inflammation, and something called ‘cellular senescence.' And we have been interested in my lab in senescence because it is a unique process that has an important role in aging, but it also has a really important role in cancer. Senescence is a cell state. Cells, when they are stressed, they respond to entering this state of senescence. The stress could come from anything. It could come from an oncogene activation. It could come from a reactive oxygen species. It could come from a direct damage to the cell. But it is a cell state, just like apoptosis, necrosis. Senescence is a state in which the cell, in response to that stressor, undergoes an arrest from the G to the S phase. And that arrest is oftentimes associated with a resistance to apoptosis. So then the cell does not die, but it is alive, and it remains metabolically active. And in fact, downstream pathways of these cell cycle inhibition of this G-to-S phase lead to the increase of these transcription factors in the chromatin and lead to the development of these pro-inflammatory factors. So these cells, which can occur in various tissues in the body, can continue to live despite having developed these changes, and then they secrete these proinflammatory molecules like cytokines, chemokines, metalloproteinases, all of these, which are called the senescence-associated secretory phenotype, or SASP. And as we age, we accumulate more and more of these cells, and our bodies are no longer able – our immune system, like macrophages and T cells – are no longer able to remove them effectively. And as we accumulate them in various organs, these organs release a lot of inflammatory cytokines, and the chronic inflammation in that tissue leads to the tissue being damaged, and it does not work as well, and then it starts to decline in function. And that is believed to be how senescence plays a role in aging. It is the accumulation of senescent cells that occurs with increased damage and then the repair mechanism of clearing these cells effectively, which then leads to build up of inflammation and chronic inflammation leads up to damage in multiple tissues. Dr. Monty Pal: This concept to me is fascinating. And I guess the big question is – senescence is bad, right – is it not reasonable to think that this body of research, I mean, if you are able to sort of have a meaningful impact on senescence, it could have implications well beyond oncology. Is that fair? You really could extend lifespan all around. Is that reasonable to think, all-cause mortality? Dr. Mina Sedrak: One hundred percent. And that is what they have been shown in animal models. And the reason senescence is exciting is because it turns out that you can target these cells and you can induce apoptosis of these cells, but it requires active targeting of various pathways, but it can occur. And when it does, and it is done either genetically or pharmacologically in mice, we see that the mice can reverse damage. So if you take an old mouse and you genetically engineer it to remove senescent cells, that mouse will go from being frail to fit. And if you take a young mouse and you induce senescent cells at a high rate and you accumulate them in that mouse, that mouse, even though it is young, will become frail.  So that has really led to this exciting opportunity of, can we translate this finding that we are seeing in animals and in in vivo cells, cell cultures, into humans? And could that have a benefit beyond just one disease? Could it have a benefit in multiple diseases? And not just really longevity, which I think it would be great, but what people are really looking for is, how do we live healthy as we get older? How do we move the curve so that people are not developing chronic diseases in their 60s, but they are developing them in their 80s towards shortening the period of their life with disability rather than what we have currently, which is people are living to 70s, the average life expectancy is in the mid-70s, but they are spending 10 or 11 years in disability of that life. And so, how could we reduce that time frame? Dr. Monty Pal: This is brilliant, Mina. And for our audience, this compelling dialogue that we have had here thankfully is translating to funding for Mina's work. He just scored in the second percentile for his NIH R01 based on this topic. We are so, so proud of you. I mean, it is just remarkable work. It is not easy in the current climate to get funding, and a second percentile score is just absolutely wonderful. You know, Mina, I could probably go on with you for a couple more hours here talking about your work in cancer and aging. I think I am going to have to have you back on the podcast here. But a million thanks for sharing your thoughts here today on the ASCO Daily News Podcast.  And thanks to our listeners too. If you value the insights that you heard today on the ASCO Daily News Podcast, please do not forget to rate, review, and subscribe wherever you get your podcasts. Thanks, Mina. Dr. Mina Sedrak: Thank you so much. Disclaimer: The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement. Find out more about today's speakers:     Dr. Sumanta (Monty) Pal   @montypal  Dr. Mina Sedrak @minasedrakmd   Follow ASCO on social media:      @ASCO on Twitter     ASCO on Bluesky    ASCO on Facebook      ASCO on LinkedIn      Disclosures:     Dr. Monty Pal:    Speakers' Bureau: MJH Life Sciences, IntrisiQ, Peerview   Research Funding (Inst.): Exelixis, Merck, Osel, Genentech, Crispr Therapeutics, Adicet Bio, ArsenalBio, Xencor, Miyarsian Pharmaceutical   Travel, Accommodations, Expenses: Crispr Therapeutics, Ipsen, Exelixis   Dr. Mina Sedrak: Patents, Royalties, Other Intellectual Property: Up-to-Date

Elemental Altus Royalties and current CEO, Frederick Bell, sits down with MSD to chat about the announced merger with EMX Royalties. The deal is being back by new board members from Tether and will create a new mid-tier royalty company in the mining space. Fred discusses the merging of business strategies and cultures in the new company.

Top musicians are taking their music off Spotify and leaving the platform behind – but why? Kiwi musicians like Tiki Taane and The Bats have joined overseas acts like Deerhoof and King Gizzard & The Lizard Wizard in boycotting the platform, accusing it of exploitation, poor royalties, and subsidising big international acts. As it stands, each stream earns an artist around one-twentieth of a New Zealand cent. Tech commentator Paul Spain told Mike Hosking artists are making a fair point, as Spotify has been increasing their prices, but not artist payouts. LISTEN ABOVE See omnystudio.com/listener for privacy information.

Mining giant BHP announced yesterday that it will sack 750 workers in Queensland and suspend low-margin operations. BHP Mitsubishi Alliance Asset President Adam Lancey joined Peter Fegan on 4BC Breakfast to explain exactly why the company has had to make this decision.See omnystudio.com/listener for privacy information.

Wyoming made billions from coal mining over the last 50 years, funding the government, schools, roads, parks. But President Trump's major spending bill, passed in July, gives mining companies a break on royalty fees — leaving state budgets lean. In this episode, easing coal fees comes at a price. Plus: Non-store retail spending saw double-digit year-over-year growth, small businesses suffer as they wait for tariff clarity, and stock investors basically ignore all the bad economic headlines.Every story has an economic angle. Want some in your inbox? Subscribe to our daily or weekly newsletter.Marketplace is more than a radio show. Check out our original reporting and financial literacy content at marketplace.org — and consider making an investment in our future.

Wyoming made billions from coal mining over the last 50 years, funding the government, schools, roads, parks. But President Trump's major spending bill, passed in July, gives mining companies a break on royalty fees — leaving state budgets lean. In this episode, easing coal fees comes at a price. Plus: Non-store retail spending saw double-digit year-over-year growth, small businesses suffer as they wait for tariff clarity, and stock investors basically ignore all the bad economic headlines.Every story has an economic angle. Want some in your inbox? Subscribe to our daily or weekly newsletter.Marketplace is more than a radio show. Check out our original reporting and financial literacy content at marketplace.org — and consider making an investment in our future.

It's a gritty reboot for Remember ShuffleJoin the patreon to listen to the 2nd part of this episode on Die Another Day (coming later this week) ⁠https://www.patreon.com/c/RememberShuffleGive Remember Shuffle a follow on Twitter⁠⁠⁠⁠⁠ And on Instagram⁠⁠⁠⁠ ⁠@RememberShufflePod⁠⁠⁠⁠⁠ to interact with the show between episodes. It also makes it easier to book guests. 

Your weekly guide to the music biz and how it all works. In this week's The Price of Music: an urgent-ish delve into the news that Morrissey has announced he wants to sell his ownership of The Smiths' songs… including a suggestion from Steve and Stu about how Johnny Marr might buy the songs off Morrissey via a gmail address that Morrissey put online.And then Steve and Stu take a deep dive into a fantastic question from listener Simon who asked: artists often say that they are not making enough money from music streaming but are artists REALLY worse off today in the music streaming age?To answer this, Steve and Stu wander down some... interesting pathways. They:talk to their Top Secret Sources in the artist and label world, and found out the answer… (which may surprise you);hypothesise about both Mazzy Star AND Bonnie Tyler's record contracts;chat to Spotify, which reveals to our dynamic duo about how much they paid Mazzy Star and Bonnie Tyler(!);wonder how being a ‘radio artist' pays compared to a ‘streaming artist';dig into artist deals: because the money paid from streaming doesn't go to the artist first;ask why the artists who ARE doing well from streaming platforms aren't talking about it?…and tangentially… is TPOM better to listen to on a treadmill than Hi-NRG house music? A brief discussion.And in the special post-show lock-in section just for our Patreon Superfans, Steve and Stuart prop themselves at the bar to chat about:The time Steve worked in a record shop for a day; and he immediately faced a quandary: which letter should he file PJ Harvey under?Steve gently chides Stu over his love of a Songs Of The Summer Stats List from TikTok, which includes a load of old nostalgia songsRadiohead are back – and how do you sell tickets to shows that will be massively-oversubscribed and make sure those tickets get to real fans?After Covid's impact, money spent on live music is up - and more popular than ever.  But what were Steve and Stu's first gigs after Covid?A call for your suggestions of hard-to-file records!As ever, we welcome your feedback, emails and – in particular – any questions you might have about how the music biz works!Email us: ⁠thepriceofmusicpodcast@gmail.com⁠See you next week!Steve and Stuart======Support The Price of Music on Patreon:⁠https://www.patreon.com/ThePriceofMusic⁠Follow Steve on X - @steve_lamacqFollow Stuart on X - @stuartdredgeFollow The Price of Music on X - @PriceofMusicpodFor sponsorship, email - ⁠joe@musically.com

Sting is being sued by his ex-bandmates for millions in unpaid royalties, Radiohead surprise fans by announcing their first official tour in over 7 years, the Sex Pistols are forced to cancel their upcoming North & South American tour dates due to an unexpected injury in the band, the Ronnie James Dio Stand Up and Shout for Cancer fund announces their annual Bowl for Ronnie charity event featuring Eddie Trunk and tons of musical celebrities & more!  PLUS ‘This Week in Rock & Roll History Trivia', Rock Birthdays, ‘The Best & Worst Rock Album Artwork of the Week' & so much more!Everything is up at www.rocknewsweekly.com / All socials & TikTok @rocknewsweekly Watch us LIVE, chat with us & more…Every Sunday around 2pm PST @ https://www.twitch.tv/rocknewsweeklyWatch all of our videos, interviews & subscribe at Youtube.com/@rocknewsweeklyFollow us online:Instagram.com/rocknewsweeklyFacebook.com/rocknewsweeklyTwitter.com/rocknewsweeklyTikTok.com/@rocknewsweeklyAll of our links are up at www.rocknewsweekly.com every Monday, where you canCheck it out on 8 different platforms (including Amazon Audible & Apple/Google Podcasts) #Rock #News #RockNews #RockNewsWeekly #RockNewsWeeklyPodcast #Podcast #Podcasts #Metal #HeavyMetal #Alt #Alternative #ClassicRock #70s #80s #90s #Indie #Trivia #RockTrivia #RockBirthdays #NewMusic #NewMusicReleases #Sting #ThePolice #StewartCopeland #AndySummers #SexPistols #SteveJones #RonnieJamesDio #BowlForRonnie #Radiohead #Radiohead2025Tour #Deftones #AlabamaShakes #Mudvayne #TheSmiths #MikeJoyce

In this episode I mean to talk about this summers festival season but get sidetracked by the much more interesting/boring discussion depending on your like/dislike of someone grappling with first grade math for 35 minutes as I attempt to get into what the hell live performance royalties are, does anyone ever make any and if you are a covers band....do you need permission and who gets the live mechanicals.....warning, dumb maths incomingsupport the show over at :https://patreon.com/AlanAverillPrimordial on Spotifyhttps://open.spotify.com/artist/0BZr6WHaejNA63uhZZZZek?si=yFFV8ypSSDOESUX62_0TzQsponsored by Metal Blade recordshttps://metalblade.indiemerch.com/promo code AA 2024 for 10% off your orderships worldwideFor info on my work as a booking agent go to:https://www.facebook.com/DragonProductionsOfficialor email alan@dragon-productions.comPrimordial cds/lps available fromhttps://www.metalblade.com/primordial/death metalVERMINOUS SERPENThttps://open.spotify.com/artist/54Wpl9JD0Zn4rhpBvrN2Oa?si=zOjIulHXS5y9lW1YHMhgTAdoomDREAD SOVEREIGN https://open.spotify.com/artist/60HY4pl0nbOrZA6u2QnqDN?si=sxQ5_1htR6G3WIvy1I_wXAgothAPRILMENhttps://open.spotify.com/artist/7GzLO1YJClmN5TvV4A37MJ?si=cRXSk24lQKWSqJG-B8KbWQSupport this show http://supporter.acast.com/agitators-anonymous-the-alan-averill-podcast. Hosted on Acast. See acast.com/privacy for more information.

Amazon Merch announced the roll out of three new products! I've got the royalties and the colors for the new polos, comfort colors, & quarter-zips... as well as some new colors for standard shirts!

It's here! Another Random Clippings episode! In this mini episode, I'll pull articles from my folder of stories that just don't fit anywhere else. Happy Labor Day to my USA listeners!SOURCES“Beam Up the Royalties, Shirley.” The Arizona Republic (Phoenix, Arizona), December 28, 1988. www.newspapers.com.“Citizens Fleeing Jury Seekers.” Princeton Daily Clarion (Princeton, Indiana), January 13, 1983. www.newspapers.com.“Gang of Boys Caught After Prying Open Casket in Old Cemetery Vault.” The News (Paterson, New Jersey), September 30, 1935. www.newspapers.com.“James Beard.” Wikipedia, February 22, 2025. https://en.wikipedia.org/wiki/James_Beard. “Juror Excused Because He Does Not Like Shape of Mrozek's Head.” The Seattle Star (Seattle, Washington), September 24, 1922. www.newspapers.com.“Man Fires at Snake, Shoots Off Big Toe.” San Francisco Bulletin (San Francisco, California), May 30, 1922. www.newspapers.com.“Will Wed Her Benefactor.” The Seattle Star (Seattle, Washington), September 24, 1907. www.newspapers.com.“Wins Bride After Long Court Battle.” The Inter Ocean (Chicago, Illinois), September 20, 1907. www.newspapers.com.“‘Just Returning Radio,' Says Youth In Store.” El Paso Herald-Post (El Paso, Texas), January 11, 1964. www.newspapers.com.SOUND SOURCESAl Jolson. “I'll Say She Does.” www.pixapay.com/music.InspectorJ. “Bell, Candle Damper A (H4n).wav.” November 17, 2017. www.freesound.org.Lucille Hegamin and The Dixie Daisies. “Cold Winter Blues.” www.pixabay.com/music.

On this episode of the Self-Publishing News Podcast, Dan Holloway looks at a new study on US reading habits that shows a 40 percent drop in reading for pleasure between 2003 and 2023, with possible shifts toward digital formats and functional reading. He also covers surprising findings about reading with children, the limited impact of COVID on reading trends, and the growing controversy over Audible's new royalty model. Plus, he highlights Spotify's latest audiobook experiment, a “Follow Along” feature that adds visuals to listening. Sponsors Self-Publishing News is proudly sponsored by Bookvault. Sell high-quality, print-on-demand books directly to readers worldwide and earn maximum royalties selling directly. Automate fulfillment and create stunning special editions with BookvaultBespoke. Visit Bookvault.app today for an instant quote. Self-Publishing News is also sponsored by book cover design company Miblart. They offer unlimited revisions, take no deposit to start work and you pay only when you love the final result. Get a book cover that will become your number-one marketing tool. Find more author advice, tips, and tools at our Self-publishing Author Advice Center, with a huge archive of nearly 2,000 blog posts and a handy search box to find key info on the topic you need. And, if you haven't already, we invite you to join our organization and become a self-publishing ally. About the Host Dan Holloway is a novelist, poet, and spoken word artist. He is the MC of the performance arts show The New Libertines, He competed at the National Poetry Slam final at the Royal Albert Hall. His latest collection, The Transparency of Sutures, is available on Kindle.

In this episode, we delve into Elemental Altus Royalties' impressive Q2 financial performance, spotlighting their robust cash generation strategies. David Baker, CFO of the company, walks listeners through the key highlights of the quarter and also shares on insights on year-end guidance at these elevated gold prices.

See omnystudio.com/listener for privacy information.

David Baker CFO of Elemental Altus Royalties (TSX.V:ELE) (OTCQX:ELEMF), joins me to review Q2 2025 financials, record operating cashflows, and outsized year so far of one-off payments. We also dive into a variety of royalty partner project updates, the development growth still on tap in their portfolio of royalties, and look ahead to future acquisitions.   Financial Highlights   Royalty revenue of US$9.1 million and adjusted revenue1 of US$10.5 million, up 102% on Q2 2024 Record Operating Cash Flow plus Caserones dividends of US$14.4 million, up +900% on Q2 2024 Attributable Gold Equivalent Ounces ("GEOs") of 3,184 ounces, up 73% on Q2 2024 and adjusted EBITDA of US$8.8 million, up 155% on Q2 2024 Revenue guidance increased to US$35 million to US$40 million, based on an updated US$3,000/oz gold price for 2025 US$19.7 million increase in cash in Q2 2025   Outlook   Elemental Altus remains on track to meet record guidance of 11,600 to 13,200 GEOs, translating to increased record adjusted revenue of US$35 million to US$40 million, based on a gold price of US$3,000/oz. Production is anticipated to be weighted towards the first half of the year, driven by first gold sales from the Korali-Sud royalty This guidance represents a 38% increase in GEOs and 74% year-on-year increase in adjusted revenue at the mid-point of guidance, with full exposure to higher gold prices Elemental Altus has a Normal Course Issuer Bid ("NCIB") in place to purchase up to 12,288,129 common shares in the capital of the Company   Dave and I then do a rapid-fire review of a number of royalty partner updates at Karlawinda, Caserones Korali-Sud (Diba), Bonikro, Wahgnion, Laverton, Cactus, and Mactung;  each with compelling advancement and growth opportunities.     Turning to the financial strength of Elemental Altus, Dave highlights the US$27 million in cash on hand at quarter's end, the increased revenue guidance of over US$35 million this year, upwards of US$20 million in one-off payments coming in over 2025, the $50 million credit facility on hand, and the solid strategic investor and financial backing from Tether Investments.  All of these factors position the company to review making accretive future acquisition transactions this year and moving forward.     If you have any follow up questions for Dave regarding Elemental Altus Royalties, then please email them to me at Shad@kereport.com.   In full disclosure, Shad is a shareholder of Elemental Altus Royalties at the time of this recording, and may choose to buy or sell shares at any time.   Click here to view recent news on the Elemental Altus Royalties website

Reporter Jacob Orledge investigates ND oil royalty losses, while Dr. David Herman explains how new funding could help rural hospitals weather Medicaid cuts.

Caleb Shreve, founder and CEO of Killphonic Rights, is a pioneering advocate for artist empowerment and transparency in the music industry. With a career spanning music production, publishing, and rights management, Caleb has worked with Grammy-winning talent while building a company dedicated to helping independent artists collect the royalties they're owed. His expertise bridges the gap between creative artistry and the often opaque business side of music, making him a leading voice in modernizing rights management and creating fairer revenue models for musicians worldwide.In this episode, we explore how Caleb is challenging the status quo and creating new pathways for indie artists to thrive.Key Takeaways:How “black box” royalties work—and why so much indie artist income goes unclaimed.The role NFTs and user-centric streaming models could play in reshaping music monetization.Practical steps every artist can take to protect their rights and maximize royalty collection.---→ Learn more about Caleb Shreve and Killphonic Rights at killphonicrights.com.Book an Artist Breakthrough Session with the Modern Musician team: https://apply.modernmusician.me/podcast

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A new Japanese report has estimated the earnings of Demon Slayer creator Koyoharu Gotouge, whose royalty income has reportedly reached astronomical figures.With the Demon Slayer manga surpassing 220 million copies in circulation, Gotouge's earnings from royalties are likely immense. At Kadokawa's "World Worldless Manga Contest" panel last year, it was revealed that the royalty income for most manga artists is 10%. Based on this rate, a recent report by Real Sound estimates Gotogue's income from physical comic sales alone to be approximately 10 billion yen (about US$64 million), with digital sales adding even more to that total. This figure also does not even include the ever-expanding economic sphere of the Demon Slayer franchise, which encompasses games, stage plays and merchandise, such as a recent collaboration with convenience store chain FamilyMart that sold 2.4 million items.Support The Podcast!⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠https://creators.spotify.com/pod/show/roose366/subscribe⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Follow For More Content &Streams!Science Podcast: ⁠⁠https://open.spotify.com/show/5nFXe9dPeWrMpyObyAlrnF?si=7358d1cf32cb45b7⁠⁠Youtube Gaming: ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠https://www.youtube.com/@RooseJp/videos⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Tiktok: ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠https://www.tiktok.com/@podcastonanime

Django Degree is the founder and CEO of Focus on Words, a book platform that gives authors full ownership of their work, royalties, and audience. He's also the author of “I Hope You Wake Up” and “They Lied To You,” books that dive deep into truth, identity, and how we break free from the systems that shape us. His mission is clear: help authors reclaim their voice, rebuild broken systems, and eventually use the success of that work to fund a city for foster youth and orphans across the country.

Mineral and royalty owners face unique cybersecurity risks that most people never consider. From fraudulent emails requesting banking changes to sophisticated scams targeting royalty payments, cybercriminals increasingly view mineral owners as attractive targets due to their regular income streams and valuable assets. In this essential episode, we break down the most common digital threats facing mineral owners and provide straightforward, non-technical strategies to protect your personal information, financial accounts, and royalty payments. Whether you're tech-savvy or prefer to keep things simple, you'll discover practical steps you can implement immediately to safeguard your mineral income and personal data from online criminals.  As always, links to the resources mentioned in this episode can be found in the show notes at mineralrightspodcast.com.

July 15, 2025 | Are licensing fees required or gatekeeping? In this episode of The Chain, host Nimish Gera, vice president of Biologics at Mythic Therapeutics, and Ian Wilkinson, CEO of Gamma Proteins, discuss accessing antibody discovery technology through licensing fees and royalties—and whether these fees are justified or not. Wilkinson delves into the current landscape of antibody discovery technologies, including if AI-based technology warrants fees, how royalties affect both small companies and big pharma, and his background as one of the first experts in the field who offered purely free-for-service options. He also shares what excites him about antibody engineering and beyond. Links from this episode:  Mythic Therapeutics Gamma Proteins 

Django Degree is the founder and CEO of Focus on Words, a book platform that gives authors full ownership of their work, royalties, and audience. He's also the author of “I Hope You Wake Up” and “They Lied To You,” books that dive deep into truth, identity, and how we break free from the systems that shape us. His mission is clear: help authors reclaim their voice, rebuild broken systems, and eventually use the success of that work to fund a city for foster youth and orphans across the country.

Rob Liefeld returns to the CBH podcast talking about Youngblood hitting its stride, Extreme Studios becomes a hothouse of new series: Brigade, Bloodstrike, and nearly two dozen more, all while he mentors rising talents Dan Fraga, Norm Rapmund and more. Mounting costs inside Image spark sharp discussions with Jim Lee, Todd McFarlane, and Mark Silvestri, nudging Liefeld to open Maximum Press for experiments like Battlestar Galactica and Avengelyne. He talks about his exit from Image and his stint on Marvel's Heroes  Reborn, where his Captain America made headlines amidst Marvel's bankruptcy. Recharged, he launches Awesome Comics, partners with Alan Moore for an Award‑winning Supreme, and joins Golden Age legend Joe Simon to shield Fighting American in court. A family walk through Greek ruins now feeds the mythic spark in Cable, Deadpool, and their Fortnite cameos. Royalties still arrive, proof that owning your stories keeps the dream alive, which is a lesson his friend Robert Kirkman echoes with Walking Dead and Invincible. #RobLiefeld #Youngblood #ExtremeStudios #ImageComics #CreatorRights #HeroesReborn #CaptainAmerica #MaximumPress #AlanMoore #Deadpool Support the show

Paris Panayiotopoulos, Senior Managing Director at Blackstone Life Sciences, shares how the firm's broad life sciences strategy has been advancing innovation across the life sciences ecosystem in three key ways: late-stage product financing (Collaboration) and new company creation (Ownership), and non-dilutive financing (Credit and Royalties). He explains how Blackstone is bridging the innovation funding gap through high-conviction partnerships with larger BioPharma and MedTech companies, and targeted investment in late-stage trials.

We welcome in Dan O'Flaherty, CEO of Versamet Royalties, for an introduction of the company and its portfolio of projects, which includes cash-royalties and streams. The company was brought to the market by the likes of Equinox Gold and Sandstorm. Dan shares insights into its strategy and the checklists it needs for adding additional assets to their portfolio.

Welcome to the Squared Circle Podcast! I am your host Marie Shadows, and on this episode, we are thanking the men and unpacking feminsit buzzwords.If you believe in my content and love it, support below! Your follows, shares, and upgrade to a paid membership helps out my brand and community to do more as a one-woman content maker:https://marieshadows.substack.comhttps://youtube.com/squaredcirclepodcasthttps://marieshadows-shop.fourthwall.com/https://buymeacoffee.com/marieshadowshttps://discord.gg/jMpZg5G85VMarie Shadows returns with a fiery editorial on why equality isn't what the media or wrestling fans think it is. From Bully Ray's controversial quote to personal experience inside the locker room, Marie pulls no punches on why merit, value, and gratitude matter more than slogans.

Welcome to episode 194 of Growers Daily! We cover: when your plants are ready before the soil is, why (some) farmers should get royalties, and compost tea applications.  We are a Non-Profit! 

Hey hey! Today's we've got CHANDLER BOLT of SelfPublishing.com in the studio to discuss the economics of self-publishing a book.We talk about: - The difference between self publishing and normal publishing. - How much money people make self publishing books. - AI in book publishing, how it's changing (or not changing). - The different forms of monetizing a book: Royalties vs backend. - We go through examples of 10 books and their results. - How Chandler's company did $70,000,000 of revenue so far.Follow Chandler Bolt:

EP:53 - Film Music in Flux: Royalties, AI & the Streaming Shakeup  First Step For Sync? Get Your Music Meta-Data Done Right! - Grab your FREE guide on how to do this here: https://mailchi.mp/839e030188ce/9mc45541ff   

Sean "Diddy" Combs, once a titan of music and media with a billion-dollar empire, is watching his fortune shrink under the crushing weight of mounting legal battles. Federal criminal charges, sprawling civil lawsuits, and high-profile accusations have turned his brand from gold to toxic overnight. Partnerships have been severed, business ventures frozen, and revenue streams throttled as sponsors, artists, and corporations flee the storm. What was once a sprawling Bad Boy kingdom—spanning liquor, fashion, music, and television—now resembles a crumbling fortress under siege. Legal fees alone are bleeding him dry, with elite defense teams billing by the hour while court after court keeps the fire roaring.Behind the scenes, Diddy's vast wealth is being dissected by plaintiffs, prosecutors, and investigators like vultures circling a carcass. Bank accounts are being subpoenaed, assets traced, and shell companies unraveled. Real estate holdings are under scrutiny. Royalties and intellectual property once seen as long-term goldmines are now potential collateral. The lifestyle he once flaunted—private jets, champagne nights, and mogul bravado—has been replaced with a desperate damage control operation. And as new accusers continue to step forward and civil litigation piles higher, it's becoming increasingly clear: Diddy isn't just fighting for his legacy anymore—he's fighting to keep the lights on.to contact me:bobbycapucci@protonmail.com

Sean "Diddy" Combs, once a titan of music and media with a billion-dollar empire, is watching his fortune shrink under the crushing weight of mounting legal battles. Federal criminal charges, sprawling civil lawsuits, and high-profile accusations have turned his brand from gold to toxic overnight. Partnerships have been severed, business ventures frozen, and revenue streams throttled as sponsors, artists, and corporations flee the storm. What was once a sprawling Bad Boy kingdom—spanning liquor, fashion, music, and television—now resembles a crumbling fortress under siege. Legal fees alone are bleeding him dry, with elite defense teams billing by the hour while court after court keeps the fire roaring.Behind the scenes, Diddy's vast wealth is being dissected by plaintiffs, prosecutors, and investigators like vultures circling a carcass. Bank accounts are being subpoenaed, assets traced, and shell companies unraveled. Real estate holdings are under scrutiny. Royalties and intellectual property once seen as long-term goldmines are now potential collateral. The lifestyle he once flaunted—private jets, champagne nights, and mogul bravado—has been replaced with a desperate damage control operation. And as new accusers continue to step forward and civil litigation piles higher, it's becoming increasingly clear: Diddy isn't just fighting for his legacy anymore—he's fighting to keep the lights on.to contact me:bobbycapucci@protonmail.comBecome a supporter of this podcast: https://www.spreaker.com/podcast/the-epstein-chronicles--5003294/support.

What's your intellectual property truly worth when it's on the line? Not what you hope or what you feel, but what courts, investors, and negotiators will actually pay. This episode of Intangiblia dives deep into the high-stakes world of IP valuation, where patents, trademarks, and copyrights transform from abstract legal protections into concrete dollar amounts.We journey through landmark global IP disputes that have defined how creative assets are valued in courtrooms from California to Colombia. The Samsung v. Apple design patent battle set precedent for how much of a product's profit can be attributed to its appearance. Epic Systems v. Tata Consultancy Services revealed the billion-dollar worth of trade secrets when they cross into competitors' hands. Meanwhile, cases like Liffers in Spain demonstrate that even moral rights, the right to be credited for your work, carry financial value that courts will recognize and enforce.The podcast unpacks three essential valuation methodologies that every creator should understand: cost-based (what it took to create), market-based (what others pay for similar assets), and income-based (what future earnings it will generate). Through fascinating case studies across industries, from pharmaceuticals to streaming services, sneakers to smartphones, we see how these approaches play out in real disputes with massive financial implications.Beyond methodology, we explore how valuation strategies differ across borders, with emerging economies like India pushing back against one-size-fits-all licensing rates, and Mexico's courts mandating that IP damages reflect genuine commercial impact. The digital transformation adds another layer of complexity, as shown in Disney v. Redbox, where even access codes carried enforceable intellectual property value.Whether you're protecting your creative work, licensing your technology, or facing infringement, this episode delivers a crucial message: in intellectual property, real power lies not just in registration but in pricing. Because in the world of IP, value isn't what you feel, it's what you can prove.Send us a text

Eagle Royalties and Summit Royalty Corp have entered into a definitive amalgamation agreement in respect of a reverse takeover transaction pursuant to which Summit will go public by way of the takeover of Eagle. New drill results from Kenorland Minerals, NGEx Minerals, and Collective Mining. Kingfisher commences drilling at HWY37. Snowline announced the discovery of a new gold system at Cynthia. This episode of Mining Stock Daily is brought to you by... Revival Gold is one of the largest pure gold mine developer operating in the United States. The Company is advancing the Mercur Gold Project in Utah and mine permitting preparations and ongoing exploration at the Beartrack-Arnett Gold Project located in Idaho. Revival Gold is listed on the TSX Venture Exchange under the ticker symbol “RVG” and trades on the OTCQX Market under the ticker symbol “RVLGF”. Learn more about the company at ⁠⁠⁠revival-dash-gold.com⁠⁠⁠Vizsla Silver is focused on becoming one of the world's largest single-asset silver producers through the exploration and development of the 100% owned Panuco-Copala silver-gold district in Sinaloa, Mexico. The company consolidated this historic district in 2019 and has now completed over 325,000 meters of drilling. The company has the world's largest, undeveloped high-grade silver resource. Learn more at⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ ⁠https://vizslasilvercorp.com/⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Equinox has recently completed the business combination with Calibre Mining to create an Americas-focused diversified gold producer with a portfolio of mines in five countries, anchored by two high-profile, long-life Canadian gold mines, Greenstone and Valentine. Learn more about the business and its operations at ⁠⁠⁠equinoxgold.com⁠⁠⁠ Integra is a growing precious metals producer in the Great Basin of the Western United States. Integra is focused on demonstrating profitability and operational excellence at its principal operating asset, the Florida Canyon Mine, located in Nevada. In addition, Integra is committed to advancing its flagship development-stage heap leach projects: the past producing DeLamar Project located in southwestern Idaho, and the Nevada North Project located in western Nevada. Learn more about the business and their high industry standards over at integraresources.com

Dr. Diwakar Davar and Dr. Jason Luke discuss novel agents in melanoma and other promising new data in the field of immunotherapy that were presented at the 2025 ASCO Annual Meeting. TRANSCRIPT Dr. Diwakar Davar: Hello. My name is Diwakar Davar, and I am welcoming you to the ASCO Daily News Podcast. I'm an associate professor of medicine and the clinical director of the Melanoma and Skin Cancer Program at the University of Pittsburgh's Hillman Cancer Center. Today, I'm joined by my colleague and good friend, Dr. Jason Luke. Dr. Luke is a professor of medicine. He is also the associate director of clinical research and the director of the Phase 1 IDDC Program at the University of Pittsburgh's Hillman Cancer Center. He and I are going to be discussing some key advancements in melanoma and skin cancers that were presented at the 2025 ASCO Annual Meeting. Our full disclosures are available in the transcript of this episode.  Jason, it is great to have you back on the podcast. Dr. Jason Luke: Thanks again so much for the opportunity, and I'm really looking forward to it. Dr. Diwakar Davar: Perfect. So we will go ahead and start talking a little bit about a couple of key abstracts in both the drug development immunotherapy space and the melanoma space. The first couple of abstracts, the first two, will cover melanoma. So, the first is LBA9500, which was essentially the primary results of RELATIVITY-098. RELATIVITY-098 was a phase 3 trial that compared nivolumab plus relatlimab in a fixed-dose combination against nivolumab alone for the adjuvant treatment of resected high-risk disease. Jason, do you want to maybe give us a brief context of what this is? Dr. Jason Luke: Yeah, it's great, thanks. So as almost all listeners, of course, will be aware, the use of anti–PD-1 immunotherapies really revolutionized melanoma oncology over the last 10 to 15 years. And it has become a standard of care in the adjuvant setting as well. But to review, in patients with stage III melanoma, treatment can be targeted towards BRAF with BRAF and MEK combination therapy, where that's relevant, or anti–PD-1 with nivolumab or pembrolizumab are a standard of care. And more recently, we've had the development of neoadjuvant approaches for palpable stage III disease. And in that space, if patients present, based on two different studies, either pembrolizumab or nivolumab plus ipilimumab can be given prior to surgery for somewhere in the 6- to 9-week range. And so all of these therapies have improved time-to-event endpoints, such as relapse-free or event-free survival. It's worth noting, however, that despite those advances, we've had a couple different trials now that have actually failed in this adjuvant setting, most high profile being the CheckMate-915 study, which looked at nivolumab plus ipilimumab and unfortunately was a negative study. So, with RELATIVITY-047, which was the trial of nivolumab plus relatlimab that showed an improvement in progression-free survival for metastatic disease, there's a lot of interest, and we've been awaiting these data for a long time for RELATIVITY-098, which, of course, is this adjuvant trial of LAG-3 blockade with relatlimab plus nivolumab. Dr. Diwakar Davar: Great. So with that, let's briefly discuss the trial design and the results. So this was a randomized, phase 3, blinded study, so double-blinded, so neither the investigators knew what the patients were getting, nor did the patients know what they were getting. The treatment investigational arm was nivolumab plus relatlimab in the fixed-dose combination. So that's the nivolumab standard fixed dose with relatlimab that was FDA approved in RELATIVITY-047. And the control arm was nivolumab by itself. The duration of treatment was 1 year. The patient population consisted of resected high-risk stage III or IV patients. The primary endpoint was investigator-assessed RFS. Stage and geography were the standard stratifying factors, and they were included, and most of the criteria were balanced across both arms. What we know at this point is that the 2-year RFS rate was 64% and 62% in the nivolumab and nivolumab-combination arms, respectively. The 2-year DMFS rate was similarly equivalent: 76% with nivolumab monotherapy, 73% with the combination. And similar to what you had talked about with CheckMate 915, unfortunately, the addition of LAG-3 did not appear to improve the RFS or DMFS compared to control in this patient population. So, tell us a little bit about your take on this and what do you think might be the reasons why this trial was negative? Dr. Jason Luke: It's really unfortunate that we have this negative phase 3 trial. There had been a lot of hope that the combination of nivolumab with relatlimab would be a better tolerated combination that increased the efficacy. So in the metastatic setting, we do have 047, the study that demonstrated nivolumab plus relatlimab, but now we have this negative trial in the adjuvant setting. And so as to why exactly, I think is a complicated scenario. You know, when we look at the hazard ratios for relapse-free survival, the primary endpoint, as well as the secondary endpoints for distant metastasis-free survival, we see that the hazard ratio is approximately 1. So there's basically no difference. And that really suggests that relatlimab in this setting had no impact whatsoever on therapeutic outcomes in terms of efficacy. Now, it's worth noting that there was a biomarker subanalysis that was presented in conjunction with these data that looked at some immunophenotyping, both from circulating T cells, CD8 T cells, as well as from the tumor microenvironment from patients who were treated, both in the previous metastatic trial, the RELATIVITY-047 study, and now in this adjuvant study in the RELATIVITY-098 study. And to briefly summarize those, what was identified was that T cells in advanced melanoma seemed to have higher expression levels of LAG-3 relative to T cells that are circulating in patients that are in the adjuvant setting. In addition to that, there was a suggestion that the magnitude of increase is greater in the advanced setting versus adjuvant. And the overall summary of this is that the suggested rationale for why this was a negative trial may have been that the target of LAG-3 is not expressed as highly in the adjuvant setting as it is in the metastatic setting. And so while the data that were presented, I think, support this kind of an idea, I am a little bit cautious that this is actually the reason for why the trial was negative, however. I would say we're not really sure yet as to why the trial was negative, but the fact that the hazard ratios for the major endpoints were essentially 1 suggests that there was no impact whatsoever from relatlimab. And this really makes one wonder whether or not building on anti–PD-1 in the adjuvant setting is feasible because anti–PD-1 works so well. You would think that even if the levels of LAG-3 expression were slightly different, you would have seen a trend in one direction or another by adding a second drug, relatlimab, in this scenario. So overall, I think it's an unfortunate circumstance that the trial is negative. Clearly there's going to be no role for relatlimab in the adjuvant setting. I think this really makes one wonder about the utility of LAG-3 blockade and how powerful it really can be. I think it's probably worth pointing out there's another adjuvant trial ongoing now of a different PD-1 and LAG-3 combination, and that's cemiplimab plus fianlimab, a LAG-3 antibody that's being dosed from another trial sponsor at a much higher dose, and perhaps that may make some level of difference. But certainly, these are unfortunate results that will not advance the field beyond where we were at already. Dr. Diwakar Davar: And to your point about third-generation checkpoint factors that were negative, I guess it's probably worth noting that a trial that you were involved with, KeyVibe-010, that evaluated the PD-1 TIGIT co-formulation of vibostolimab, MK-4280A, was also, unfortunately, similarly negative. So, to your point, it's not clear that all these third-generation receptors are necessarily going to have the same impact in the adjuvant setting, even if they, you know, for example, like TIGIT, and they sometimes may not even have an effect at all in the advanced cancer setting. So, we'll see what the HARMONY phase 3 trial, that's the Regeneron cemiplimab/fianlimab versus pembrolizumab control with cemiplimab with fianlimab at two different doses, we'll see how that reads out. But certainly, as you've said, LAG-3 does not, unfortunately, appear to have an impact in the adjuvant setting. So let's move on to LBA9501. This is the primary analysis of EORTC-2139-MG or the Columbus-AD trial. This was a randomized trial of encorafenib and binimetinib, which we will abbreviate as enco-bini going forward, compared to placebo in high-risk stage II setting in melanoma in patients with BRAF V600E or K mutant disease. So Jason, you know, you happen to know one or two things about the resected stage II setting, so maybe contextualize the stage II setting for us based on the trials that you've led, KEYNOTE-716, as well as CheckMate-76K, set us up to talk about Columbus-AD. Dr. Jason Luke: Thanks for that introduction, and certainly stage II disease has been something I've worked a lot on. The rationale for that has been that building off of the activity of anti–PD-1 in metastatic melanoma and then seeing the activity in stage III, like we just talked about, it was a curious circumstance that dating back about 7 to 8 years ago, there was no availability to use anti–PD-1 for high-risk stage II patients, even though the risk of recurrence and death from melanoma in the context of stage IIB and IIC melanoma is in fact similar or actually higher than in stage IIIA or IIIB, where anti–PD-1 was approved. And in that context, a couple of different trials that you alluded to, the Keynote-716 study that I led, as well as the CheckMate 76K trial, evaluated pembrolizumab and nivolumab, respectively, showing an improvement in relapse-free and distant metastasis-free survival, and both of those agents have subsequently been approved for use in the adjuvant setting by the US FDA as well as the European Medicines Agency.  So bringing then to this abstract, throughout melanoma oncology, we've seen that the impact of anti–PD-1 immunotherapy versus BRAF and MEK-targeted therapy have had very similar outcomes on a sort of comparison basis, both in frontline metastatic and then in adjuvant setting. So it was a totally reasonable question to ask: Could we use adjuvant BRAF and MEK inhibitor therapy? And I think all of us expected the answer would be yes. As we get into the discussion of the trial, I think the unfortunate circumstance was that the timing of this clinical trial being delayed somewhat, unfortunately, made it very difficult to accrue the trial, and so we're going to have to try to read through the tea leaves sort of, based on only a partially complete data set. Dr. Diwakar Davar: So, in terms of the results, they wanted to enroll 815 patients, they only enrolled 110. The RFS and DMFS were marginally improved in the treatment arm but certainly not significantly, which is not surprising because the trial had only accrued 16% to 18% of its complete accrual. As such, we really can't abstract from the stage III COMBI-AD data to stage II patients. And certainly in this setting, one would argue that the primary treatment options certainly remain either anti–PD-1 monotherapy, either with pembrolizumab or nivolumab, based on 716 or 76K, or potentially active surveillance for the patients who are not inclined to get treated.  Can you tell us a little bit about how you foresee drug development going forward in this space because, you know, for example, with HARMONY, certainly IIC disease is a part of HARMONY. We will know at least a little bit about that in this space. So what do you think about the stage IIB/C patient population? Is this a patient population in which future combinations are going to be helpful, and how would you think about where we can go forward from here? Dr. Jason Luke: It is an unfortunate circumstance that this trial could not be accrued at the pace that was necessary. I think all of us believe that the results would have been positive if they'd been able to accrue the trial. In the preliminary data set that they did disclose of that 110 patients, you know, it's clear there is a difference at a, you know, a landmark at a year. They showed a 16% difference, and that would be in line with what has been seen in stage III. And so, you know, I think it's really kind of too bad. There's really going to be no regulatory approach for this consideration. So using BRAF and MEK inhibition in stage II is not going to be part of standard practice moving into the future. To your point, though, about where will the field go? I think what we're already realizing is that in the adjuvant setting, we're really overtreating the total population. And so beyond merely staging by AJCC criteria, we need to move to biomarker selection to help inform which patients truly need the treatment. And in that regard, I don't think we've crystallized together as a field as yet, but the kinds of things that people are thinking about are the integration of molecular biomarkers like ctDNA. When it's positive, it can be very helpful, but in melanoma, we found that, unfortunately, the rates are quite low, you know, in the 10% to 15% range in the adjuvant setting. So then another consideration would be factors in the primary tumor, such as gene expression profiling or other considerations.  And so I think the future of adjuvant clinical trials will be an integration of both the standard AJCC staging system as well as some kind of overlaid molecular biomarker that helps to enrich for a higher-risk population of patients because on a high level, when you abstract out, it's just clearly the case that we're rather substantially overtreating the totality of the population, especially given that in all of our adjuvant studies to date for anti–PD-1, we have not yet shown that there's an overall survival advantage. And so some are even arguing perhaps we should even reserve treatment until patients progress. I think that's a complicated subject, and standard of care at this point is to offer adjuvant therapy, but certainly a lot more to do because many patients, you know, unfortunately, still do progress and move on to metastatic disease. Dr. Diwakar Davar: Let's transition to Abstract 2508. So we're moving on from the melanoma to the novel immunotherapy abstracts. And this is a very, very, very fascinating drug. It's IMA203. So Abstract 2508 is a phase 1 clinical update of IMA203. IMA203 is an autologous TCR-T construct targeting PRAME in patients with heavily pretreated PD-1-refractory metastatic melanoma. So Jason, in the PD-1 and CTLA-4-refractory settings, treatment options are either autologous TIL, response rate, you know, ballpark 29% to 31%, oncolytic viral therapy, RP1 with nivolumab, ORR about 30-ish percent. So new options are needed. Can you tell us a little bit about IMA203? Perhaps tell us for the audience, what is the difference between a TCR-T and traditional autologous TIL? And a little bit about this drug, IMA203, and how it distinguishes itself from the competing TIL products in the landscape. Dr. Jason Luke: I'm extremely enthusiastic about IMA203. I think that it really has transformative potential based on these results and hopefully from the phase 3 trial that's open to accrual now. So, what is IMA203? We said it's a TCR-T cell product. So what that means is that T cells are removed from a patient, and then they can be transduced through various technologies, but inserted into those T cells, we can then add a T-cell receptor that's very specific to a single antigen, and in this case, it's PRAME. So that then is contrasted quite a bit from the TIL process, which includes a surgical resection of a tumor where T cells are removed, but they're not specific necessarily to the cancer, and they're grown up in the lab and then given to the patient. They're both adoptive cell transfer products, but they're very different. One is genetically modified, and the other one is not. And so the process for generating a TCR-T cell is that patients are required to have a new biomarker that some may not be familiar with, which is HLA profiling. So the T-cell receptor requires matching to the concomitant HLA for which the peptide is bound in. And so the classic one that is used in most oncology practices is A*02:01 because approximately 48% of Caucasians have A*02:01, and the frequency of HLA in other ethnicities starts to become highly variable. But in patients who are identified to have A*02:01 genotype, we can then remove blood via leukapheresis or an apheresis product, and then insert via lentiviral transduction this T-cell receptor targeting PRAME. Patients are then brought back to the hospital where they can receive lymphodepleting chemotherapy and then receive the reinfusion of the TCR-T cells. Again, in contrast with the TIL process, however, these T cells are extremely potent, and we do not need to give high-dose interleukin-2, which is administered in the context of TIL. Given that process, we have this clinical trial in front of us now, and at ASCO, the update was from the phase 1 study, which was looking at IMA203 in an efficacy population of melanoma patients who were refractory at checkpoint blockade and actually multiple lines of therapy. So here, there were 33 patients and a response rate of approximately 50% was observed in this population of patients, notably with a duration of response approximately a year in that treatment group. And I realize that these were heavily pretreated patients who had a range of very high-risk features. And approximately half the population had uveal melanoma, which people may be aware is a generally speaking more difficult-to-treat subtype of melanoma that metastasizes to the liver, which again has been a site of resistance to cancer immunotherapy. So these results are extremely promising. To summarize them from what I said, it's easier to make TCR-T cells because we can remove blood from the patient to transduce the T cells, and we don't have to put them through surgery. We can then infuse them, and based on these results, it looks like the response rate to IMA203 is a little bit more than double what we expect from lifileucel. And then, whereas with lifileucel or TILs, we have to give high-dose IL-2, here we do not have to give high-dose IL-2. And so that's pretty promising. And a clinical trial is ongoing now called the SUPREME phase 3 clinical trial, which is hoping to validate these results in a randomized global study. Dr. Diwakar Davar: Now, one thing that I wanted to go over with you, because you know this trial particularly well, is what you think of the likelihood of success, and then we'll talk a little bit about the trial design. But in your mind, do you think that this is a trial that has got a reasonable likelihood of success, maybe even a high likelihood of success? And maybe let's contextualize that to say an alternative trial, such as, for example, the TebeAM trial, which is essentially a T-cell bispecific targeting GP100. It's being compared against SOC, investigator's choice control, also in a similarly heavily pretreated patient population. Dr. Jason Luke: So both trials, I think, have a strong chance of success. They are very different kinds of agents. And so the CD3 bispecific that you referred to, tebentafusp, likely has an effect of delaying progression, which in patients with advanced disease could have a value that might manifest as overall survival. With TCR-T cells, by contrast, we see a very high response rate with some of the patients going into very durable long-term benefit. And so I do think that the SUPREME clinical trial has a very high chance of success. It will be the first clinical trial in solid tumor oncology randomizing patients to receive a cell therapy as compared with a standard of care. And within that standard of care control arm, TILs are allowed as a treatment. And so it will also be the first study that will compare TCR-T cells against TILs in a randomized phase 3. But going back to the data that we've seen in the phase 1 trial, what we observe is that the duration of response is really connected to the quality of the response, meaning if you have more than a 50% tumor shrinkage, those patients do very, very well. But even in patients who have less than 50% tumor shrinkage, the median progression-free survival right now is about 4.5 months. And again, as we think about trial design, standard of care options for patients who are in this situation are unfortunately very bad. And the progression-free survival in that population is probably more like 2 months. So this is a trial that has a very high likelihood of being positive because the possibility of long-term response is there, but even for patients who don't get a durable response, they're likely going to benefit more than they would have based on standard chemotherapy or retreatment with an anti–PD-1 agent. Dr. Diwakar Davar: Really, a very important trial to enroll, a trial that is first in many ways. First of a new generation of TCR-T agents, first trial to look at cell therapy in the control arm, a new standard of efficacy, but potentially also if this trial is successful, it will also be a new standard of trial conduct, a new kind of trial, of a set of trials that will be done in the second-line immunotherapy-refractory space. So let's pivot to the last trial that we were going to discuss, which was Abstract 2501. Abstract 2501 is a first-in-human phase 1/2 trial evaluating BNT142, which is the first-in-class mRNA-encoded bispecific targeting Claudin-6 and CD3 in patients with Claudin-positive tumors. We'll talk a little bit about this, but maybe let's start by talking a little bit about Claudin-6. So Claudin-6 is a very interesting new target. It's a target that's highly expressed in GI and ovarian tumors. There are a whole plethora of Claudin-6-targeting agents, including T-cell bispecifics and Claudin-6-directed CAR-Ts that are being developed. But BNT142 is novel. It's a novel lipid nanoparticle LNP-encapsulated mRNA. The mRNA encodes an anti–Claudin-6 CD3 bispecific termed RiboMAB-021. And it then is administered to the patient. The BNT142-encoding mRNA LNPs are taken up by the liver and translated into the active drug. So Jason, tell us a little bit about this agent. Why you think it's novel, if you think it's novel, and let's talk a little bit then about the results. Dr. Jason Luke: So I certainly think this is a novel agent, and I think this is just the first of what will probably become a new paradigm in oncology drug development. And so you alluded to this, but just to rehash it quickly, the drug is encoded as genetic information that's placed in the lipid nanoparticle and then is infused into the patient. And after the lipid nanoparticles are taken up by the liver, which is the most common place that LNPs are usually taken up, that genetic material in the mRNA starts to be translated into the actual protein, and that protein is the drug. So this is in vivo generation, so the patient is making their own drug inside their body. I think it's a really, really interesting approach. So for any drug that could be encoded as a genetic sequence, and in this case, it's a bispecific, as you mentioned, CD3-Claudin-6 engager, this could have a tremendous impact on how we think about pharmacology and novel drug development moving into the future in oncology. So I think it's an extremely interesting drug, the like of which we'll probably see only more moving forward. Dr. Diwakar Davar: Let's maybe briefly talk about the results. You know, the patient population was heavily pretreated, 65 or so patients, mostly ovarian cancer. Two-thirds of the patients were ovarian cancer, the rest were germ cell and lung cancer patients. But let's talk a little bit about the efficacy. The disease control rate was about 58% in the phase 1 population as a whole, but 75% in the ovarian patient population. Now tell us a little bit about the interesting things about the drug in terms of the pharmacokinetics, and also then maybe we can pivot to the clinical activity by dose level. Dr. Jason Luke: Well, so they did present in their presentation at ASCO a proportionality showing that as higher doses were administered, that greater amounts of the drug were being made inside the patient. And so that's an interesting observation, and it's an important one, right? Suggesting that the pharmacology that we classically think of by administering drugs by IV, for example, would still be in play. And that did translate into some level of efficacy, particularly at the higher dose levels. Now, the caveat that I'll make a note of is that disease control rate is an endpoint that I think we have to be careful about because what that really means is sometimes a little bit unclear. Sometimes patients have slowly growing tumors and so on and so forth. And the clinical relevance of disease control, if it doesn't last at least 6 months, I think is probably pretty questionable. So I think these are extremely interesting data, and there's some preliminary sense that getting the dose up is going to matter because the treatment responses were mostly observed at the highest dose levels. There's also a caveat, however, that across the field of CD3 bispecific molecules like this, there's been quite a bit of heterogeneity in terms of the response rate, with some of them only really generating stable disease responses and other ones having more robust responses. And so I think this is a really interesting initial foray into this space. My best understanding is this molecule is not moving forward further after this, but I think that this really does set it up to be able to chase after multiple different drug targets on a CD3 bispecific backbone, both in ovarian cancer, but then basically across all of oncology. Dr. Diwakar Davar: Perfect. This is a very new sort of exciting arena where we're going to be looking at, in many ways, these programmable constructs, whether we're looking at in vivo-generated, in this case, a T-cell bispecific, but we've also got newer drugs where we are essentially giving drugs where people are generating in vivo CAR T, and also potentially even in vivo TCR-T. But certainly lots of new excitement around this entire class of drugs. And so, what we'd like to do at this point in time is switch to essentially the fact that we've got a very, very exciting set of data at ASCO 2025. You've heard from Dr. Luke regarding the advances in both early drug development but also in advanced cutaneous melanoma. And Jason, as always, thank you so much for sharing your very valuable and great, fantastic insights with us on the ASCO Daily News Podcast. Dr. Jason Luke: Well, thanks again for the opportunity. Dr. Diwakar Davar: And thank you to our listeners for taking your time to listen today. You will find the links to the abstracts that we discussed today in the transcript of this episode. And finally, if you value the insights that you hear on the ASCO Daily News Podcast, please take a moment to rate, review, and subscribe wherever you get your podcasts. Disclaimer: The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement. Follow today's speakers:    Dr. Diwakar Davar    @diwakardavar    Dr. Jason Luke @jasonlukemd Follow ASCO on social media:     @ASCO on Twitter       ASCO on Bluesky   ASCO on Facebook       ASCO on LinkedIn   Disclosures:     Dr. Diwakar Davar:      Honoraria: Merck, Tesaro, Array BioPharma, Immunocore, Instil Bio, Vedanta Biosciences     Consulting or Advisory Role: Instil Bio, Vedanta Biosciences     Consulting or Advisory Role (Immediate family member): Shionogi     Research Funding: Merck, Checkmate Pharmaceuticals, CellSight Technologies, GSK, Merck, Arvus Biosciences, Arcus Biosciences     Research Funding (Inst.): Zucero Therapeutics     Patents, Royalties, Other Intellectual Property: Application No.: 63/124,231 Title: COMPOSITIONS AND METHODS FOR TREATING CANCER Applicant: University of Pittsburgh–Of the Commonwealth System of Higher Education Inventors: Diwakar Davar Filing Date: December 11, 2020 Country: United States MCC Reference: 10504-059PV1 Your Reference: 05545; and Application No.: 63/208,719 Enteric Microbiotype Signatures of Immune-related Adverse Events and Response in Relation to Anti-PD-1 Immunotherapy     Dr. Jason Luke:     Stock and Other Ownership Interests: Actym Therapeutics, Mavu Pharmaceutical, Pyxis, Alphamab Oncology, Tempest Therapeutics, Kanaph Therapeutics, Onc.AI, Arch Oncology, Stipe, NeoTX     Consulting or Advisory Role: Bristol-Myers Squibb, Merck, EMD Serono, Novartis, 7 Hills Pharma, Janssen, Reflexion Medical, Tempest Therapeutics, Alphamab Oncology, Spring Bank, Abbvie, Astellas Pharma, Bayer, Incyte, Mersana, Partner Therapeutics, Synlogic, Eisai, Werewolf, Ribon Therapeutics, Checkmate Pharmaceuticals, CStone Pharmaceuticals, Nektar, Regeneron, Rubius, Tesaro, Xilio, Xencor, Alnylam, Crown Bioscience, Flame Biosciences, Genentech, Kadmon, KSQ Therapeutics, Immunocore, Inzen, Pfizer, Silicon Therapeutics, TRex Bio, Bright Peak, Onc.AI, STipe, Codiak Biosciences, Day One Therapeutics, Endeavor, Gilead Sciences, Hotspot Therapeutics, SERVIER, STINGthera, Synthekine     Research Funding (Inst.): Merck , Bristol-Myers Squibb, Incyte, Corvus Pharmaceuticals, Abbvie, Macrogenics, Xencor, Array BioPharma, Agios, Astellas Pharma , EMD Serono, Immatics, Kadmon, Moderna Therapeutics, Nektar, Spring bank, Trishula, KAHR Medical, Fstar, Genmab, Ikena Oncology, Numab, Replimmune, Rubius Therapeutics, Synlogic, Takeda, Tizona Therapeutics, Inc., BioNTech AG, Scholar Rock, Next Cure     Patents, Royalties, Other Intellectual Property: Serial #15/612,657 (Cancer Immunotherapy), and Serial #PCT/US18/36052 (Microbiome Biomarkers for Anti-PD-1/PD-L1 Responsiveness: Diagnostic, Prognostic and Therapeutic Uses Thereof)     Travel, Accommodations, Expenses: Bristol-Myers Squibb, Array BioPharma, EMD Serono, Janssen, Merck, Novartis, Reflexion Medical, Mersana, Pyxis, Xilio

Are you a founder thinking about writing a book? This video unpacks how to leverage your expertise for long-term income, going beyond just royalties! Join us as we reveal the secrets to a successful book-writing and publishing journey. In this episode, discover: Why a book is essential for founders: Learn how a book can be a powerful tool for solving real-world problems for people in your business, enhancing credibility, and generating deal flow.Different book types and how to get started: Understand the distinction between a "handbook" and an "idea book," and why a handbook is often the best starting point for experts. You'll hear practical tips on how to use existing content like webinars or speeches, even with AI, to quickly create a book.Publishing strategies: Explore the differences between self-publishing, hybrid, and traditional publishing, and which might be best for you. Find out that while traditional publishers can handle licensing and foreign language rights, promotion ultimately remains your responsibility.The realistic timeline and process: Learn that writing and promoting a solid book takes about a year—six months for writing (starting with a book proposal for market validation) and six months for heavy promotion, often via podcasts.Monetizing your book: Discover that the real money-maker isn't royalties, but rather deal flow and attracting the right clients to your business by providing access to tools and funnels. The importance of thinking about your monetization strategy before you start writing is emphasized.Common mistakes to avoid: Hear about the pitfalls first-time authors often encounter, such as trying to put too much information into one book (instead of a series) and not time-blocking for writing.Don't miss these invaluable insights into turning your expertise into a valuable asset! Like, share, and subscribe for more business strategies. Join the community: For more in-depth strategies and support from Simon Severino and 217+ sprinters, join the Sprint Club at strategysprints.com – try it free for 7 days!

Mining Stock Daily interviews Fred Bell, CEO of Elemental Altus Royalties, discussing the recent acquisition of a majority stake by Tether and its implications for the gold royalty business. The discussion covers the rapid developments leading to this deal, the strategic growth opportunities it presents, and the transformative impact on access to capital. The conversation also touches on the democratization of gold investment through Tether's stable coin and the recent changes in the company's board structure.

This week on the New Music Business podcast, Ari sits down with Oscar Höglund, the co-founder and CEO of Epidemic Sound. Epidemic Sound is a leading music and soundtracking platform for content creators. They have garnered attention for its digital rights model and soundtracking tools that help creators to elevate their content with music, while simultaneously supporting artists financially. Oscar shares insights from his journey launching Epidemic after working with Sweden's renowned Zodiak Television.In their episode, Ari and Oscar unpack critical issues impacting independent artists, including royalty structures, streaming economics, and the evolving landscape of music licensing. They explore Epidemic Sound's unique approach to artist compensation, discuss how digital streaming has pushed music toward playlist-driven consumption, and tackle the creative tension artists face when making commercially viable music. This episode offers an in-depth look at one of the industry's most influential platforms shaping the future of music in content creation.Chapters00:00 The Changing Landscape of Music Royalties06:00 Epidemic Sound: A New Model for Music Distribution12:14 Artist Compensation and Ownership Rights17:46 Innovative Approaches to Music Licensing24:09 The Impact of Epidemic Sound on Independent Artists29:53 Future of Music in the Digital Age42:16 The Evolution of Music Consumption46:21 Negotiating with DSPs and Licensing Rates49:52 The Rise of Epidemic Sound55:31 The Artist's Identity Crisis01:08:01 Future Innovations and AI in Music01:21:12 Becoming a Full-Service Music PlatformEdited and mixed by Ari DavidsMusic by Brassroots DistrictProduced by the team at Ari's TakeOrder the THIRD EDITION of How to Make It in the New Music Business: https://book.aristake.com Hosted on Acast. See acast.com/privacy for more information.

Normally a years old social media video might come back to HAUNT you, but for today’s Phone Tap victim, that kind of video might change his life for GOOD!See omnystudio.com/listener for privacy information.

Normally a years old social media video might come back to HAUNT you, but for today’s Phone Tap victim, that kind of video might change his life for GOOD!See omnystudio.com/listener for privacy information.