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USA Today
3 days ago
- Health
- USA Today
A potential new treatment for Parkinson's shows early promise
A potential new treatment for Parkinson's shows early promise | The Excerpt On a special episode (first released on May 29, 2025) of The Excerpt podcast: Parkinson's is a disease that afflicts an estimated 90,000 Americans every year. Dr. Lorenz Studer and Dr. Viviane Tabar of Memorial Sloan Kettering Cancer Center, joined USA TODAY The Excerpt to share more about a new stem cell-based therapy that creates nerve cells. The treatment is showing early promise. Hit play on the player below to hear the podcast and follow along with the transcript beneath it. This transcript was automatically generated, and then edited for clarity in its current form. There may be some differences between the audio and the text. Podcasts: True crime, in-depth interviews and more USA TODAY podcasts right here Karen Weintraub: Hello, and welcome to The Excerpt. I'm USA TODAY Health Reporter Karen Weintraub. Today is Thursday, May 29th, and this is a special episode of The Excerpt. You've no doubt heard of the chemical dopamine. It's often referenced as part of the brain's reward system when we do something pleasurable. Dopamine, or a lack thereof, also plays a critical role in the onset of Parkinson's, a disease that afflicts an estimated 90,000 Americans every year. Treatment for Parkinson's focuses on managing its many symptoms, as there is no cure. But a new stem cell therapy developed at Memorial Sloan Kettering Cancer Center for advanced Parkinson's is showing early promise. What's behind this incredible discovery and just how hopeful should patients be? Here to talk about this exciting new treatment and its impact on patients are the two physicians who helped make it a reality. Dr. Viviane Tabar and Dr. Lorenz Studer. Drs. Tabar and Studer, thanks so much for joining The Excerpt. Dr. Tabar, when someone is diagnosed with Parkinson's disease, what exactly is happening to their brain and their body? Dr. Viviane Tabar: Well, we think that at the time an individual is diagnosed with Parkinson's disease, they have already experienced degeneration or loss of a large number of their dopamine neurons. We are all born with a limited number of large, beautiful dopamine neurons that live in our brainstem and that project to multiple areas in the brain. They're involved in a lot of intricate activities, but an important element of their function is to modulate movement. So the individual very commonly will come to clinical attention because of movement difficulties, albeit there are other symptoms, loss of smell, gastrointestinal symptoms, difficulties with sleep, and it's a complex picture. But it's important to remember that at the time they receive this diagnosis, which today is still vastly made on a clinical basis, on an examination of the individual and listening to their symptoms, they have already lost probably 50% or more of their dopamine neurons and their projections. A potential new treatment for Parkinson's shows early promise A new stem cell-based therapy creates cells that make dopamine, a chemical that's critical to the disease. Karen Weintraub: And what are some of the everyday challenges your patients face? You mentioned motor control, cognitive issues also I think? Dr. Viviane Tabar: For the majority of patients, and keep in mind that Parkinson's is a disease that spans a variety of symptoms and spectrum of progression and intensity, for most patients it starts with manageable symptoms that they control well, could be a tremor, could be some stiffness in their gait. And for the majority, I would say cognitive change comes late, assuming a proper diagnosis of Parkinson's. So it becomes paradoxically even more problematic because it starts interfering with activities of daily living, your ability to get to and from your job. You're still high-performing, but you are impaired gradually. And you're fully cognitively there often, and so you're very aware of the slow degeneration that's essentially relentless. Karen Weintraub: And you mentioned jobs. Are people affected by Parkinson's primarily older, retiree age, or are there other groups at risk as well? Dr. Viviane Tabar: We didn't say necessarily retirees. Parkinson's, the sporadic form of it, which is the most common form, I mean by that the form that's not inherited, that happens commonly in the sixties or later. But nowadays, people in their fifties and sixties are considered at their prime still at work. Karen Weintraub: And others who are affected, we think of Michael J. Fox who is certainly younger when he started developing symptoms. Dr. Viviane Tabar: There are forms of Parkinson's that occur in a younger individual at a younger average age, and that is commonly related to specific mutations. And so the majority of Parkinson's disease occurs what we call sporadically, so without a hereditary or identified specific mutation that we are aware of. But some is related to a mutation, and those tend to occur at a younger age, but that's not the majority. Karen Weintraub: And is it clear what causes Parkinson's? You mentioned the neurons, but is there still some mystery there, and can the causes vary from person to person? Dr. Viviane Tabar: There is a lot of mystery. So in simple terms, we do not know the etiology of Parkinson's disease very specifically. Many things have been invoked, the environment, environmental toxins, a genetic predisposition outside of the genetic forms of the disease. And we can talk a lot about some exciting science trying to dissect what's going on, the role of inflammation, et cetera. But the short answer to your question is we're not able today to tell a patient what caused their Parkinson's, again, outside the relatively uncommon hereditary forms. Karen Weintraub: And can you walk us a little bit through how Parkinson's progresses over time? Is there a sort of a path, many paths, what does that look like? Dr. Viviane Tabar: So yes, there are many paths, but let's take an average situation. The patient would reach out to a physician, eventually come to the attention of a neurologist, they're examined, their brain scan is obtained. In the case of Parkinson's, often that scan is fine and normal to age and the symptoms are identified often, as we said earlier, motor symptoms. The common situation is that they get started on a form of dopamine that can reach the brain, and that makes them feel better and that is often referred to as the honeymoon period. And that goes on for a few years where the patient is almost back to normal but dependent on the medicine. And as time goes by, the disease process is such that they are losing more and more of their dopamine neurons. And at some point we start or the treating neurologist starts escalating the dose of the medication. And there are other medications that can support that. But essentially within a few years or several years depending, they reach a point where they're starting to experience side effects from the medication and a shortening of the periods where they are feeling okay and functioning. And that is where we start getting stuck in that there are no new medications that, I shouldn't say no new medications, there's always new medications, no formulations that try to extend the ability to help the individual. But you clearly plateau in terms of the effectiveness of pharmacological therapy for a lot of patients, not all. There are options that are surgical like inserting electrodes that is called deep brain stimulation, which will work for some patients. But we reach a point where the patient has lost most of their dopaminergic neurons and there is not much more that can be offered today to help the individual. Hence, the idea of what if we could replace those degenerated dopamine neurons? Karen Weintraub: Which brings us to Dr. Studer. Dr. Studer, when did you first think about using stem cells as a possible way to treat Parkinson's? Dr. Lorenz Studer: Well, it's really a very long story. In fact, it's I think nearly three decades when we first had the idea of doing so, which was the question, "Now, can we really replace cells in the brain and what will be the right source?" In fact, that was the goal of my laboratory starting 25 years ago, finding exactly what's the source of dopamine neurons. The challenge is how do you make this very, very specific nerve cell in the brain? And so that was a long journey, took us at least 10 years of basic research to understand, now what is the code of development? It's a little bit like trying to go through the steps that the cells go in normal development, but give them those signals one by one in a culture dish. And so it's a little bit like a code that we need to decipher and then to apply to the cells. And by 2011, we could do that finally in a study that showed that we did a good job because when we implant those cells back into a mouse, in a rat or in a monkey model of Parkinson's disease, we see benefit in that model. And that really then opened up the whole next new step, now can we do that not just in a animal model, but maybe eventually in humans? That was what they call the proof of concept. But then obviously it was not a long journey to get to the ultimate clinical patient. Karen Weintraub: And how might the stem cell therapies transform the treatment landscape? What opportunities does this offer? And are there specific symptoms that you expect to get better or everything or certain symptoms? Dr. Lorenz Studer: The dopamine acts primarily on the movement-related symptoms. That's the area where we think we can make the biggest impact. Whether it's also going to affect all the symptoms, it's more questionable. Now, for example, again, we said the patients can have loss of smell, they can have problems with severe constipation, and at later stage of the disease, cognitive issues. And at this point we don't have a good reason to believe that this therapy will also help with those symptoms. This has to be tested. It could be indirect effects, but the main effect we expect is that the movement disorder should improve. Again, we don't want to overstate it, but in a dream scenario, it would be you have still Parkinson's disease, so you cannot cure Parkinson's disease, but maybe if it worked, ideally you could cure the movement disorder component of Parkinson's disease. And so I think that's really what we are trying to develop with this type of cell therapy. And maybe in the future this will open up the same approach for all the cell types that might affect all the symptoms as well. So it's also kind of opening up the door to many other cell therapies in Parkinson's itself and maybe in other diseases as well, because it's one of the first cases now where really you actually replacing nerve cells in the brain, which sounds like a little bit of a science fiction approach. But I think this is one of the first examples where we really tried to attempt that and hopefully opening the door now for applications in the future. Karen Weintraub: And you said we can't call this a cure, obviously it's early days, but what would it take to get to a cure? More cell types? Dr. Lorenz Studer: Yeah. I think, because again, Parkinson's has more than just a movement disorder. So all that's not just movement-related, there is late stages cognitive problems, gastrointestinal problems, sleep problems, and those are unlikely to be treated with this cell type. So what you can envisage is yes, well, maybe you would have additional cell types that can attack that, or ideally, you brought that up now, what causes Parkinson's disease, it'll be a complementary approach where you would give the cells back, because many dopamine cells are already lost by the time you're diagnosed. So you get that movement-related symptoms hopefully restored, but at the same time, you'll find, like the whole field, many thousands researchers try to do that, find a therapy that can slow down or stop the progression. So you would gain back the function that you've already lost, but you would maybe not get some of those later symptoms. That would be even bigger dream in the future. Karen Weintraub: I was going to ask, Dr. Studer, where the research goes from here? Dr. Lorenz Studer: We always talk about bench to bedside, but there's also a bedside to bench. So where you kind of try to figure out, so what could you do even better now with regard to the cells that they function maybe more quickly or they are more potent or they have some additional features like we discussed? How could it treat some of the other symptoms in the future? So I think that's a big area for Parkinson's disease itself. How can we get the most benefit out of this kind of an approach? But then the other part is really there's so many other very severe diseases now. We talk about Alzheimer's disease, we talk about ELS and other disorders. Each of them might need a different approach, quite different. So in some case we don't think we can just replace nerve cells, but we still learn that maybe other approaches could be used in those specific disorders. And it then gives us a lot of encouragement when we see some progress in one area that this might be not just kind of a one-time go, but we might have opportunities to now give some help to those very difficult to treat neurodegenerative disorders where even today, this has been kind of some of the value of this for many of the drugs. Now, very, very few new drugs came up in the context of neurodegenerative disorders, and I don't think cell therapy is alone going to solve all of that, but it's yet the new tool that is becoming actually clinically a realistic option to replace cells, and I think that's quite exciting. There's some examples, for example, for treating eye disorders, so-called people who get blindness, macular degeneration, where data look quite promising. There's some examples maybe in very severe seizures where [inaudible 00:12:35] could be useful. So I think this is one of the very, very first example now where we now go all the way to this phase three study, but in the lab now we are thinking, "What did we learn? Why did it take us 25 years, for example? How can you make it quicker and what would be some of the next targets?" Because from the stem cell side, we learned a lot. So by now we can pretty much make any cell type of the brain. So that's a language to make this as no longer limiting. What's limiting is now to know what's really needed in each individual patient, which is going to be quite distinct and will take, again, a couple of years, but pretty confident not another 25-year step. Karen Weintraub: Well, we will stay tuned for that very exciting work. Thank you both so much for being on The Excerpt. Dr. Lorenz Studer: Thanks so much. Dr. Viviane Tabar: Thank you for having us. Karen Weintraub: Thanks to our senior producers, Shannon Rae Green and Kaely Monahan, for their production assistance. Our executive producer is Laura Beatty. Let us know what you think of this episode by sending a note to podcasts@ Thanks for listening. I'm USA TODAY Health Reporter Karen Weintraub. Taylor Wilson will be back tomorrow morning with another episode of The Excerpt.
Business Wire
3 days ago
- Health
- Business Wire
CAR T Vision Coalition Launches with Ambitious Goal to Double Patients Treated with the Curative Potential of CAR T-cell Therapy by 2030
CHICAGO--(BUSINESS WIRE)--Today an international coalition announces the launch of CAR T Vision to unite stakeholders around the shared ambition that every eligible patient should have the opportunity for cure with CAR T-cell therapy. By 2030, the aim is to double the proportion of eligible patients treated with CAR T-cell therapy. As outlined in the new roadmap report, the coalition will work to address access challenges and drive meaningful change in the CAR T-cell therapy healthcare ecosystem with a focus on three critical priorities: increasing awareness and understanding of CAR T-cell therapy; expanding resources and capacity to deliver CAR T-cell therapy; and developing sustainable and innovative financing approaches to manage the costs of treatment and care. The CAR T Vision is for every eligible patient to have the opportunity for cure with CAR T-cell therapy. By 2030, the aim is to double the proportion of eligible patients treated with CAR T-cell therapy. 'Despite CAR T-cell therapy being available in the United States for nearly seven years in large B-cell lymphoma, only approximately two out of 10 eligible patients with some advanced blood cancers ever receive CAR T-cell therapy,' said Miguel Perales, MD, Chief, Adult Bone Marrow Transplantation Service, Memorial Sloan Kettering Cancer Center (MSK); Past President, American Society for Transplantation and Cellular Therapy (ASTCT); and Co-Chair, CAR T Vision Steering Committee. 'When it comes to treating these potentially deadly cancers, every minute counts. That is why we established CAR T Vision with recommendations for interventions that, when adopted and scaled, will help many more eligible patients get the opportunity for cure within the next five years.' The roadmap report, developed by an independent Steering Committee comprised of leadership from top North American and European patient advocacy groups, medical society organizations, academic and community treatment centers, health technology assessment, policy, and other subject matter experts, provides the foundations for advocacy and action by local stakeholders to address the specific access challenges patients face in different geographies. Building on the report, expert Working Groups will be established to translate the Vision into concrete, measurable actions, including specific recommendations and a measurement framework to track progress. 'Limited awareness of CAR T-cell therapy, low referrals, hospital capacity challenges, and funding and reimbursement are among the barriers that either prevent people from accessing CAR T-cell therapy altogether or cause delays that advance a patient's cancer beyond the point of treatment eligibility. In short, these barriers cost lives,' said Anna Sureda, MD, PhD, Clinical Hematologist, Professor and Cell Therapy Researcher; and Co-Chair, CAR T Vision Steering Committee. 'We call on every stakeholder and organization with the ability to help shape better patient outcomes—policymakers, health system leaders, payors, healthcare providers, patient advocates, and industry—to join the growing coalition of Vision endorsers and help ensure every eligible patient has the opportunity for cure with CAR T-cell therapy.' Making CAR T Vision a reality will require the coming together of a complex ecosystem of partners, each with their own unique role to play. To learn more about CAR T Vision, review the roadmap report and join the coalition, visit About CAR T-cell therapy and CAR T Vision CAR T-cell therapy involves engineering a person's own immune cells to target and treat cancer and is currently approved for certain types of aggressive blood cancers, enabling some patients to remain cancer free for more than five years. 4,5,6,7 The CAR T Vision is for every eligible patient to have the opportunity for cure with CAR T-cell therapy. By 2030, the aim is to double the proportion of eligible patients treated with CAR T-cell therapy. The CAR T Vision Steering Committee includes leadership from top North American and European patient advocacy groups, medical society organizations, academic and community treatment centers, health technology assessment, policy, and other subject matter experts. The new roadmap report details the challenges CAR T Vision aims to resolve through multidisciplinary collaboration and the urgent actions needed to make the Vision a reality. The report and initial activities of the CAR T Vision Steering Committee have been funded by Gilead Sciences and Kite, as the inaugural supporter of CAR T Vision. Report content has been reviewed by Gilead Sciences and Kite. However, the Steering Committee has editorial control of the CAR T Vision and its outputs, including the report. Dr. Perales has financial interests related to Gilead Sciences and Kite. To learn more about CAR T Vision, review the report and join the growing coalition of endorsers, visit 1 Kaltwasser J. Investigators set sights on optimizing CAR T-cell therapy in lymphoma. OncLive. 2022. Available online: 2 Chuhara, D, Liao, L, et al. Real-world experience of CAR T-cell therapy in older patients with relapsed/refractory diffuse large B-cell lymphoma. Blood. 2023, September 21. 3 Canales Albendea MÁ, Canonico PL, Cartron G, et al. Comparative analysis of CAR T-cell therapy access for DLBCL patients: associated challenges and solutions in the four largest EU countries. Front Med (Lausanne). 4 Abramson J, Palomba ML, Gordon LI, et al. Five-Year Survival of Patients (pts) from Transcend NHL 001 (TRANSCEND) Supports Curative Potential of Lisocabtagene Maraleucel (liso-cel) in Relapsed or Refractory (R/R) Large B-Cell Lymphoma (LBCL). Blood. 2024;144(1):3125. 5 Neelapu SS, Jacobson CA, Ghobadi A, et al. Five-year follow-up of ZUMA-1 supports the curative potential of axicabtagene ciloleucel in refractory large B-cell lymphoma. Blood. 2023 May 11;141(19):2307-2315. doi: 10.1182/blood.2022018893. PMID: 36821768; PMCID: PMC10646788. 6 Rives S, Maude S, Hiramatsu H et al. S112: TISAGENLECLEUCEL IN PEDIATRIC AND YOUNG ADULT PATIENTS (PTS) WITH RELAPSED/REFRACTORY (R/R) B-CELL ACUTE LYMPHOBLASTIC LEUKEMIA (B-ALL): FINAL ANALYSES FROM THE ELIANA STUDY. HemaSphere 6():p 13-14, June 2022. | DOI: 10.1097/ 7 Xu J, Wang BY, Yu SH, et al. Long-term remission and survival in patients with relapsed or refractory multiple myeloma after treatment with LCAR-B38M CAR T cells: 5-year follow-up of the LEGEND-2 trial. J Hematol Oncol. 2024 Apr 24;17(1):23. doi: 10.1186/s13045-024-01530-z. PMID: 38659046; PMCID: PMC11040812.
Medscape
4 days ago
- Health
- Medscape
Defying Grim Prognosis to Celebrate a 20th ‘Cancerversary'
In 2005, Roy Brosgole, then 38, was a busy working parent. He commuted about an hour each way to a teaching job in New York City and took care of his children — then 4 years and almost 2 years — in the evenings. His lifestyle then kept him sitting in the car for hours daily, so it didn't surprise him that his back often ached. One morning Brosgole got up, went to the bathroom, coughed, and then found himself lying flat on the floor in blinding pain. After he tried and failed to stand, his wife Lori called 9-1-1. In the emergency room, Brosgole was triaged and — without any imaging — diagnosed with back spasms. He recalled that the attending physician ordered a strong steroid and pain meds, but neither of these treatments helped relieve the intense discomfort. 'The doctor said, 'Wow that's really strange. You should be able to get up and walk around now.' I said, 'Well, I can't.' The doctor's exact words — I will never forget them: 'Don't worry about it. It's not like you have back cancer or anything,' Brosgole recalled, in an interview. A few days later, an MRI ordered by Brosgole's orthopedist would prove the emergency room physician's statement wrong. The imaging of Brosgole's back showed a plasmacytoma on his sacrum, which doctors told him could be a precursor to multiple myeloma or lymphoma. 'The tumor was growing into the sacrum like Swiss cheese,' Brosgole said. He then consulted Patrick Boland, MD, an orthopedic surgeon at Memorial Sloan Kettering Cancer Center (MSKCC) in New York City. His appointment fell on a Tuesday, he was admitted immediately, and his tumor was removed the next day. Brosgole was diagnosed with IgG kappa multiple myeloma, International Staging System stage II. His myeloma carried two chromosomal abnormalities, deletion 13 and deletion 17p, both associated with aggressive disease and poorer long-term prognosis. Brosgole's condition was designated as high risk, so he was told he might have only a few years to live. Fast forward to 2025, as Brosgole is celebrating his 20-year 'cancerversary.' He credits his survival to clinical trials and new standards of care for myeloma. Chemotherapy and Stem Cell Transplants: Finding a Balance Multiple myeloma was fairly uncommon in 2005, when Brosgole was diagnosed. Today, the disease is more prevalent but still rare. About 36,000 people will be diagnosed with multiple myeloma in 2025— 20,030 men and 16,080 women. The disease currently has a 62% 5-year survival rate. When Brosgole was diagnosed, the 5-year survival rate was 56% for patients younger than 65 years and significantly lower for people with chromosomal deletions, like him. Once the tumor was excised, Brosgole was put on a regimen of dexamethasone and thalidomide, alternating 4 days on and 4 days off. The treatments brought his cancer markers down significantly, but his doctors, noting that he was young and otherwise healthy, offered him the chance to participate in a clinical trial of tandem stem cell transplants. The study would assess if such treatment could improve long-term survival as compared with a single autologous stem cell transplant. The first transplant took place in November 2005, with Brosgole's doctor harvesting his stem cells. Next, he underwent high-dose chemotherapy. Just 3 months later, in February 2006, he went through the entire process again. That treatment was successful for 18 months, he said. 'Then all of a sudden, my numbers — M spike protein levels, immunoglobulins, protein electrophoresis — started to climb,' Brosgole said. When his MSKCC oncologist agreed that he had relapsed, Brosgole was started on a new intravenous chemotherapy cocktail of Velcade (bortezomib) and Revlimid (lenalidomide) with dexamethasone. That treatment worked for a while, too. His tumor markers stayed stable for nearly a year, but his MSKCC care team wanted to add another treatment: Allogenic bone marrow transplant. That procedure took place in May 2011. In the years since then, Brosgole's cancer has often recurred, but donor lymphocyte infusions (DLIs) have brought him back into remission. 'I had 10 DLIs: December 2011, April 2012, September 2012, March 2013, November 2013, January 2014, August 2015, September 2015, and November 2015,' Brosgole noted. He was also given an immunomodulatory agent, lenalidomide, which he took until March 2021. Then he transitioned to a different immunotherapy drug, Pomalyst. Today Brosgole has no detectible levels of multiple myeloma in his body. 'If you do a blood test, there's no way you could tell that I ever had multiple myeloma,' he said. Treatment for Multiple Myeloma: 2025 When you look back at Brosgole's earlier treatments, they differ significantly from today's standard of care, said Hamza Hashmi, MD, a hematologist-oncologist at MSKCC. Hashmi, Brosgole's current doctor, said that allogenic bone marrow transplant comes with the risk for graph-vs-host disease. 'The mortality rate of allogeneic transplant procedures is somewhere around 30-40%,' Hashmi explained. 'Back in 2011, we were pursuing heroic measures for patients like Roy in their 40s, hoping to put myeloma into a deep and durable remission. Someone who is diagnosed today with multiple myeloma would start with a four-drug cocktail of chemotherapy — combinations of chemo and immunotherapies that target the cancer in a very intuitive way that can actually lead to very deep, durable remissions.' If patients relapse, they move on to chimeric antigen receptor (CAR) T-cell therapy, which was first FDA-approved in 2017 for treatment of acute childhood lymphoblastic leukemia. 'It has shown very promising efficacy, with very tolerable or minimal toxicity or side effects, in comparison to the allogenic transplant, which can be very difficult to go through, especially if a patient is elderly, frail, or has many different comorbidities,' Hashmi explained. Other drugs on the horizon may push the needle even further. One new drug, teclistamab, is already helping patients who have stopped responding to three previous therapies or treatments. A phase 2 clinical trial, published in The New England Journal of Medicine in June 2022, found that nearly 40% of study patients saw complete eradication of their disease. In addition, monoclonal antibodies such as daratumumab are added to the standard-of-care drug combinations. Finally, bispecific antibody drug treatments, which recognize antigens on both the patient's T-cells and the myeloma cells, are shrinking tumors for people who stop responding to other treatments. Unlike CAR T-cell therapy, which requires removal and manipulation of the patient's T cells, bispecific antibody treatments are available immediately. These innovative treatments have transformed life expectancy, Hashmi said. 'In 2025 we are saying that average survival for a myeloma patient is beyond 15-20 years. And when I say survival, I mean a 70-year-old man, so you can imagine if someone is 40 years old when they get diagnosed, they may actually be able to live another 30-plus years of their life with their cancer in control and remission,' he said.
Yahoo
5 days ago
- Business
- Yahoo
Y-mAbs Therapeutics, Inc. (YMAB) Unveils Promising Cancer Trial Data at ANR 2025
Y-mAbs Therapeutics, Inc. (NASDAQ:YMAB) has presented the early-stage clinical data from its GD2-SADA PRIT trial at the Advances in Neuroblastoma Research (ANR) Meeting in Washington, D.C. The presentation marks a significant update in its experimental pipeline. The trial-in-progress poster contained findings from Trial 1001, a Phase 1 study assessing GD2-SADA Pretargeted Radioimmunotherapy using 177Lu-DOTA in patients with high-risk neuroblastoma and other GD2-expressing tumors. A scientist in a lab coat, holding a beaker of a biopharmaceutical creation. The focus of the company's presentation was on radioimmunotherapy innovation. The GD2-SADA construct, developed in a partnership with Memorial Sloan Kettering Cancer Center, deploys a two-step process allowing localized irradiation of tumors while limiting off-target toxicity. Trial 1001 has now completed Part A and has identified the optimal dosage for the GD2-SADA protein. It is currently being prepared for further evaluation. Y-mAbs Therapeutics, Inc. (NASDAQ:YMAB) has scheduled to deliver its initial data readout during its virtual R&D update on May 28. The company's stock gained 5.37% in the past week right before the new unveiling, reflecting investor confidence in Y-mAbs Therapeutics, Inc. (NASDAQ:YMAB)'s proprietary Self-Assembly DisAssembly (SADA) platform as well as the upcoming clinical milestones. Analysts remain bullish, offering a consensus Buy rating, while projecting an average price target of $16.50 with an upside potential of 281.94%. While we acknowledge the potential of YMAB as an investment, our conviction lies in the belief that some AI stocks hold greater promise for delivering higher returns and have limited downside risk. If you are looking for an AI stock that is more promising than YMAB and that has 100x upside potential, check out our report about the READ NEXT: 10 Unstoppable Dividend Stocks to Buy Now and 11 Oversold Global Stocks to Buy According to Hedge Funds Disclosure: None. Sign in to access your portfolio
Yahoo
6 days ago
- Business
- Yahoo
Y-mAbs Therapeutics, Inc. (YMAB) Unveils Promising Cancer Trial Data at ANR 2025
Y-mAbs Therapeutics, Inc. (NASDAQ:YMAB) has presented the early-stage clinical data from its GD2-SADA PRIT trial at the Advances in Neuroblastoma Research (ANR) Meeting in Washington, D.C. The presentation marks a significant update in its experimental pipeline. The trial-in-progress poster contained findings from Trial 1001, a Phase 1 study assessing GD2-SADA Pretargeted Radioimmunotherapy using 177Lu-DOTA in patients with high-risk neuroblastoma and other GD2-expressing tumors. A scientist in a lab coat, holding a beaker of a biopharmaceutical creation. The focus of the company's presentation was on radioimmunotherapy innovation. The GD2-SADA construct, developed in a partnership with Memorial Sloan Kettering Cancer Center, deploys a two-step process allowing localized irradiation of tumors while limiting off-target toxicity. Trial 1001 has now completed Part A and has identified the optimal dosage for the GD2-SADA protein. It is currently being prepared for further evaluation. Y-mAbs Therapeutics, Inc. (NASDAQ:YMAB) has scheduled to deliver its initial data readout during its virtual R&D update on May 28. The company's stock gained 5.37% in the past week right before the new unveiling, reflecting investor confidence in Y-mAbs Therapeutics, Inc. (NASDAQ:YMAB)'s proprietary Self-Assembly DisAssembly (SADA) platform as well as the upcoming clinical milestones. Analysts remain bullish, offering a consensus Buy rating, while projecting an average price target of $16.50 with an upside potential of 281.94%. While we acknowledge the potential of YMAB as an investment, our conviction lies in the belief that some AI stocks hold greater promise for delivering higher returns and have limited downside risk. If you are looking for an AI stock that is more promising than YMAB and that has 100x upside potential, check out our report about the READ NEXT: 10 Unstoppable Dividend Stocks to Buy Now and 11 Oversold Global Stocks to Buy According to Hedge Funds Disclosure: None. Error while retrieving data Sign in to access your portfolio Error while retrieving data Error while retrieving data Error while retrieving data Error while retrieving data
