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New Study Shows Arima Genomics’ Technology Detects Actionable Cancer Drivers in Solid Tumors Missed by Standard Tests

On April 10, 2025 Arima Genomics, Inc. (Arima), a company leveraging 3D genomics to reveal actionable insights that will empower researchers and clinicians to improve human health, reported the publication of a study in The Journal of Molecular Diagnostics showing its proprietary technology detected clinical structural variants missed by conventional clinical tests (Press release, Arima Genomics, APR 10, 2025, View Source [SID1234651881]). Conducted in collaboration with researchers from NYU Langone Health, Weill Cornell School of Medicine, Scripps Cancer Center, Moores Cancer Center at the University of California, San Diego, and the University of Colorado School of Medicine, the retrospective study found that Arima’s technology identified gene fusions or rearrangements in 71% of cases where standard molecular techniques failed. Importantly, in 14% of these cases where no driver had been found by other techniques, a clinically actionable variant was identified.

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"Structural variants like gene fusions are central to cancer diagnostics, but current clinical tests miss many events that are crucial to diagnostic and therapeutic decision-making," said Matija Snuderl, MD, Professor of Pathology and Director of Molecular Pathology and Diagnostics at NYU Langone Health and corresponding author of the study. "Arima’s technology allowed us to detect hidden variants — many of them clinically actionable — in cases where standard tests came up empty. This provided important information to our understanding of the cancers and directly impacted patient care in some cases, confirming diagnoses and improving treatment options."

In the current study, researchers analyzed 71 formalin-fixed, paraffin-embedded (FFPE) specimens across ten solid tumor types, comparing results using Arima’s technology to results from prior clinical testing via fluorescence in situ hybridization (FISH), RNA sequencing, and DNA sequencing. Arima’s technology demonstrated 98% concordance with positive cases detected by conventional methods. Among the 14 samples negative by standard techniques, structural variants in 71% (10/14) were uncovered. Among these:

14% (2/14) harbored gene fusions or rearrangements listed in current clinical guidelines, directly impacting patient care.
14% (2/14) involved rearrangements affecting therapeutically targetable genes, potentially expanding treatment options even though they are not currently classified as actionable in guidelines.
Several cases described in the paper highlight the utility of Arima’s technology in achieving proper diagnosis and enabling appropriate therapeutic intervention.

For example, one young patient experiencing seizures was initially believed to have a non-tumorous brain abnormality called focal cortical dysplasia. DNA methylation results hinted at a possible low-grade glioma but remained inconclusive following two commercial RNA sequencing panels, which did not identify a diagnostic fusion for low-grade glioma. Only when the patient’s sample was analyzed with Arima’s technology did doctors detect a MYBL1::MAML2 fusion, confirming a low-grade glioma diagnosis and allowing the patient to receive the proper treatment.

In another case involving a pediatric glioblastoma patient, Arima’s technology detected a complex rearrangement involving PD-L1 that standard RNA and DNA tests missed. Later confirmatory testing using immunohistochemistry showed that PD-L1 was overexpressed on the tumor cells and provided an opportunity for immunotherapy treatment based on PD-L1 expression—an option that would have been overlooked without the enhanced sensitivity of Arima’s technology.

Arima’s technology uses high-throughput chromosome conformation capture (Hi-C) sequencing to map the spatial architecture of the genome within FFPE tumor samples. By revealing how DNA is organized in 3D space, it detects gene fusions, rearrangements, and translocations with 100-1000 times higher signal compared to standard methods like RNA or DNA sequencing or FISH, resulting in superior sensitivity.

Beyond actionable findings, the study also described how Arima’s technology offers deep insights into tumor biology by detecting complex genomic rearrangements such chromothripsis and extrachromosomal DNA (ecDNA). Recent literature has suggested ecDNA may be involved in treatment resistance, but may also be targetable with on-market therapies.

"Our technology provides a unique method to amplify the signal of rearrangements," said Anthony Schmitt, PhD, Senior Vice President of Science at Arima Genomics. "This allows us to capture structural rearrangements with far greater sensitivity and detail in FFPE samples—bringing both immediate clinical benefit and new avenues for research."

This new publication adds to a growing body of clinical evidence supporting Arima’s technology, building on recent studies conducted in collaboration with institutions such as Yale School of Medicine, Harvard Medical School, and Seattle Children’s Hospital.

Alterome Therapeutics Announces New Chief Executive Officer and Chair of the Board of Directors

On April 10, 2025 Alterome Therapeutics, Inc., a clinical-stage biopharmaceutical company pioneering the development of next-generation, small molecule targeted therapies for the treatment of cancer, reported the appointment of Jung Choi as Chief Executive Officer (CEO) and Richard Heyman, Ph.D., as Chair of the Board of Directors (Press release, Alterome Therapeutics, APR 10, 2025, View Source [SID1234651880]).

Ms. Choi brings significant experience in growing companies from privately held, preclinical to publicly traded, commercial-stage organizations. Dr. Heyman is a scientist and entrepreneur with more than 25 years of experience in co-founding and building biotech and life science companies.

"Jung’s deep experience in building innovative portfolios and effectively scaling organizations will be invaluable to Alterome as we advance our two clinical-stage precision oncology programs from early clinical development towards commercialization. We are thrilled to welcome Jung to lead our next phase of growth and Rich to an expanded role as Chair. He has been instrumental in advising the company from our discovery phase to clinical development, and we look forward to his continued guidance," said Melissa McCracken, Partner at Nextech Ventures and member of the Board of Directors at Alterome Therapeutics. "The company thanks co-founder and former CEO Eric Murphy for his contributions to Alterome, and we are grateful for his service and leadership."

"I am honored to join the Alterome team at this important phase, as we work to advance two potential best-in-class and first-in-class treatment options for cancer patients and maximize the impact of our entire portfolio," said Ms. Choi. "My career has been driven by a passion to make transformative changes in people’s lives by delivering the best medicines science can create, and I see a great opportunity to bring this passion to life with the team at Alterome."

Ms. Choi is an expert in strategic deal making, having led or managed more than 50 transactions exceeding $17 billion in value. Her leadership experience includes serving most recently as Entrepreneur-in-Residence at Third Rock Ventures. Previously, she was Chief Business & Strategy Officer at Global Blood Therapeutics, where she was instrumental in building the company from preclinical stage to commercialization, establishing a portfolio of therapeutic hematology candidates, and leading the company’s $5.4 billion acquisition by Pfizer. She previously served as head of corporate development at InterMune (acquired by Roche), Chimerix, and Gilead Sciences, and began her career at Bay City Capital and McKinsey. She currently serves on the Boards of Annexon Biosciences and New York Blood Center.

Dr. Heyman takes the role of Chair of the Board of Directors after serving as a senior advisor to the company since 2022 and has more than 25 years of experience building oncology companies. Most recently, he served as Chair of Vividion Therapeutics, Rayze Bio and Amunix Pharma. Previously, Heyman was the Co-Founder and CEO of Aragon and Seragon Pharmaceuticals. Johnson & Johnson purchased Aragon in 2013, and Genentech purchased Seragon one year later. Dr. Heyman is the Co-Founder and Chair of ORIC Pharmaceuticals, a Venture Partner for Arch Ventures, and a Science Partner at Nextech Invest. He is also Chair of PMV Pharma and Enliven Therapeutics.

"I have had the privilege of experiencing up close Alterome’s progress since the inception of the company, as the team advanced from concept to discovery to clinical development in record time," said Dr. Heyman. "The collective experience and unwavering focus at Alterome, along with the strong support of investors, has enabled the development of two extremely promising clinical candidates with the potential to make a significant impact on the oncology therapeutic landscape."

OS Therapies Announces Positive Data for OST-HER2 in the Treatment of Unresected Osteosarcoma in Dogs Opening the Potential for Use as Front-Line Therapy in Humans

On April 10, 2025 OS Therapies (NYSE-A: OSTX) ("OS Therapies" or "the Company"), a clinical-stage immunotherapy and Antibody Drug Conjugate (ADC) biopharmaceutical company, reported positive data in the prevention or delay of amputation during the treatment of primary osteosarcoma for OST-HER2 combined palliative radiation in dogs with unresected appendicular osteosarcoma (Press release, OS Therapies, APR 10, 2025, View Source [SID1234651879]). The treatment led to clinical and radiographic arrest of the primary tumor and prolonged time to metastasis in dogs without surgery or chemotherapy. The data opens the potential for OST-HER2 to be used in frontline therapy in human osteosarcoma prior to initiation of chemotherapy, and potentially reduce the need for chemotherapy altogether, for the purposes of preventing or delaying limb amputation or primary tumor resection surgeries, in addition to the prevention, delay and/or control of lung metastasis.

Additionally, the Company announced the publication of positive data in the journal "Molecular Therapy" entitled "Immunological responses and clinical outcomes in dogs with osteosarcoma receiving standard therapy and a Listeria vaccine expressing HER2" demonstrated the correlation of innate and adaptive immune responses to OST-HER2, with prevention of metastasis and long-term survival benefit when used in the adjuvant setting, following standard of care amputation and chemotherapy.

Treatment with OST-HER2 was found to be safe and well tolerated in both studies. Taken together, the data support the potential of OST-HER2 to achieve progression free survival (PFS) of primary osteosarcoma, prevent or delay or metastatic disease, prolong progression free survival (PFS) in metastatic disease, and significantly improve long term survival in patients with osteosarcoma. The data on the use of OST-HER2 in unresected primary osteosarcoma in dogs is being prepared for peer-reviewed publication.

"We first published strong clinical data on the benefit of OST-HER2 in canine osteosarcoma in 2016, and that led to an initial conditional approval based on a prior manufacturing process that was suboptimal for widespread veterinary use," said Dr. Nicola Mason, the Paul A. James and Charles A. Gilmore Endowed Professor at the University of Pennsylvania, School of Veterinary Medical. "Based upon this initial research, OS Therapies conducted a successful translational Phase 2b clinical trial in the rare pediatric indication of prevention of recurrence of fully resected, osteosarcoma lung metastases. Our newly published canine data and unpublished radiation combination canine data expands the potential use of OST-HER2 into delay/prevention of metastasis and PFS following resected primary osteosarcoma and raises the intriguing possibility of combination radiation therapy and OST-HER2 in the treatment of unresectable osteosarcoma."

The Company is preparing to submit this data to USDA, along with new data generated on its newly patented, commercially superior manufacturing process, with the aim of gaining conditional approval for the new manufacturing process for OST-HER2 in the United States to begin sales in 2025. Thereafter, the Company intends to conduct a pivotal clinical study with the aim of gaining full approval in 2026. A link to the publication is available here: View Source(25)00113-3.

"It has been my dream since founding the Company that OST-HER2 could potentially change the standard of care in osteosarcoma, potentially limiting the need for amputation or surgical resection of the primary tumor," said Paul Romness, CEO of OS Therapies. "With today’s data, we believe we are taking the first steps towards this given that our Comparative Oncology approach, as a result of the 96% genetic homology between human and canine osteosarcoma, leads us to believe there is significant potential for this canine data to translate into humans in the treatment of frontline and primary metastatic osteosarcoma, similarly to how it has in recurrent, fully-resected, lung metastatic osteosarcoma."

Mr. Romness continued, "We are laser focused on getting an Accelerated Approval for OST-HER2 in recurrent, fully resected, lung metastatic human osteosarcoma via Accelerated Approval by year-end 2025 and then using funds obtained from the sale of our pending Priority Review Voucher to expand the potential clinical uses of OST-HER2 throughout the human osteosarcoma treatment paradigm. In parallel, we believe the data from these two studies support the use of OST-HER2 in all phases of canine osteosarcoma treatment and we are hopeful to obtain conditional approval with our newly improved, patented manufacturing for OST-HER2 later this year so that we can launch the product at specialized cancer centers and our four-legged patients can begin getting treatment very soon.

U.S. FDA Grants Full Approval of VITRAKVI® (larotrectinib) for Adult and Pediatric Patients with NTRK Gene Fusion-Positive Solid Tumors

On April 10, 2025 Bayer reported that the U.S. Food and Drug Administration (FDA) has granted full approval for VITRAKVI (larotrectinib), a first-in-class TRK inhibitor for the treatment of adult and pediatric patients with solid tumors that have a neurotrophic receptor tyrosine kinase (NTRK) gene fusion without a known acquired resistance mutation, are metastatic or where surgical resection is likely to result in severe morbidity, and have no satisfactory alternative treatments or that have progressed following treatment (Press release, Bayer, APR 10, 2025, View Source [SID1234651878]).1 VITRAKVI has demonstrated clinically meaningful and durable responses across a range of NTRK fusion-positive solid tumors. VITRAKVI was first granted accelerated approval by FDA in November 2018.1

"This first full approval of an NTRK inhibitor by the FDA represents the culmination of research and dedication by the Bayer team," said Chandra Goda, Executive Director, U.S. VITRAKVI Brand Lead. "We are proud to deliver on our promise for patients with this significant step forward, providing a treatment option for pediatric and adult patients living with NTRK gene fusion-positive cancers. This milestone reinforces Bayer’s commitment to delivering innovative solutions that address the unique needs of patients and their families."

"The full approval of VITRAKVI by the FDA is a welcome step forward, solidifying its place as a treatment option for patients with NTRK gene fusion-positive cancers," said Andrea Ferris, President and CEO, LUNGevity Foundation. "This milestone not only benefits patients today but also paves the way for further advancements in NTRK gene therapies in the future."

This approval is based on data from three multicenter, open-label, single-arm clinical trials: LOXO-TRK-14001 (NCT02122913), SCOUT (NCT02637687), and NAVIGATE (NCT02576431). This analysis included pediatric and adult patients with unresectable or metastatic solid tumors with an NTRK gene fusion (n=339). All patients were required to have progressed following systemic therapy for their disease, if available, or would have required surgery with significant morbidity for locally advanced disease.1 The major efficacy outcome measures were overall response rate (ORR) and duration of response (DOR), as determined by a blinded independent review committee (BIRC) according to RECIST v1.1. 1 Safety was assessed in 444 patients across the three trials.1

Pooled efficacy results showed an ORR of 60% (95% CI: 55%-65%) with a complete response (CR) rate of 24% and a partial response (PR) rate of 36%.1 Five percent of patients with complete response were pathological complete response. Patients undergoing a surgical resection whose post-operative pathologic assessment showed no viable tumor cells and negative margins were pathological complete responders provided that no other sites of disease were present. Median DOR was 43.3 months (95% CI: 32.5-NE (not evaluable)).1 The most common (≥20%) adverse reactions, including laboratory abnormalities, with VITRAKVI were increased AST, increased ALT, anemia, hypoalbuminemia, musculoskeletal pain, increased alkaline phosphatase, leukopenia, lymphopenia, neutropenia, hypocalcemia, fatigue, vomiting, cough, constipation, pyrexia, diarrhea, nausea, abdominal pain, dizziness, and rash.1 Serious adverse events (AEs) reported included central nervous system (CNS) problems, bone fractures and liver problems.1

About VITRAKVI (larotrectinib)

VITRAKVI, a first-in-class oral TRK inhibitor, was exclusively designed to inhibit against the TRK family of proteins (TRKA, TRKB, and TRKC). In in vitro and in vivo tumor models, VITRAKVI demonstrated anti-tumor activity in cells with constitutive activation of TRK proteins resulting from gene fusions, deletion of a protein regulatory domain, or in cells with TRK protein overexpression. Constitutively-activated chimeric TRK fusion proteins can act as an oncogenic driver, promoting cell proliferation and survival in tumor cell lines.1

In the U.S., VITRAKVI is approved for the treatment of adult and pediatric patients with solid tumors that display a neurotrophic receptor tyrosine kinase (NTRK) gene fusion.1 Following the acquisition of Loxo Oncology by Eli Lilly and Company in February 2019, Bayer has obtained the exclusive licensing rights for the global development and commercialization, including in the U.S., for VITRAKVI.

INDICATION

VITRAKVI is indicated for the treatment of adult and pediatric patients with solid tumors that:

have a neurotrophic receptor tyrosine kinase (NTRK) gene fusion without a known acquired resistance mutation,
are metastatic or where surgical resection is likely to result in severe morbidity, and
have no satisfactory alternative treatments or that have progressed following treatment.
Select patients for therapy based on an FDA-approved test.

IMPORTANT SAFETY INFORMATION

Warnings and Precautions

Central Nervous System Effects: Central nervous system (CNS) adverse reactions occurred in patients receiving VITRAKVI, including dizziness, cognitive impairment, mood disorders, and sleep disturbances.

In patients who received VITRAKVI, all grades CNS effects including cognitive impairment, mood disorders, dizziness and sleep disorders were observed in 40.3% with Grades 3-4 in 3.8% of patients.

Cognitive impairment occurred in 11% of patients. The median time to onset of cognitive impairment was 6 months (range: 2 days to 56 months). Cognitive impairment occurring in ≥ 1% of patients included memory impairment (4.1%), disturbance in attention (3.6%), confusional state (2.3%), cognitive disorder (1.6%), delirium (1.4%), and hallucination (1.1%). Grade 3 cognitive adverse reactions occurred in 1.8% of patients and Grade 4 cognitive adverse reactions in 0.2% of patients. Among the 49 patients with cognitive impairment, 6% required a dose modification and 18% required dose interruption.

Mood disorders occurred in 14% of patients. The median time to onset of mood disorders was 3.3 months (range: 1 day to 65 months). Mood disorders occurring in ≥1% of patients included anxiety (5%), agitation (3.2%), depression (3.2%), irritability (2.3%), and restlessness (1.1%). Grade 3 mood disorders occurred in 0.9% of patients. Among the 63 patients who experienced mood disorders, no patient required a dose modification, and 1.6% required dose interruption.

Dizziness occurred in 22% of patients, and Grade 3 dizziness occurred in 0.9% of patients. Among the 96 patients who experienced dizziness, 6% of patients required a dose modification and 5% required dose interruption.
Sleep disturbances occurred in 12% of patients. Sleep disturbances included insomnia (9%), somnolence (3.4%), and sleep disorder (0.5%). Grade 3 sleep disturbances occurred in 0.2% of patients. Among the 54 patients who experienced sleep disturbances, no patient required a dose modification and 3.7% required dose interruption.

Advise patients and caretakers of these risks with VITRAKVI. Advise patients not to drive or operate hazardous machinery if they are experiencing neurologic adverse reactions. Withhold or permanently discontinue VITRAKVI based on the severity. If withheld, modify the VITRAKVI dosage when resumed.

Skeletal Fractures: Skeletal fractures can occur in patients taking VITRAKVI.

Among 444 patients who received VITRAKVI across clinical trials, fractures occurred in 7% of patients; 6% of 290 adult patients and 10% of 154 pediatric patients. Median time to first fracture was 13 months (range 27 days to 73 months) in patients followed per fracture. The most common fractures were of the rib (1.4%), fibula, foot or wrist (0.7% each). Most fractures were associated with minimal or moderate trauma. Some fractures were associated with radiologic abnormalities suggestive of local tumor involvement. VITRAKVI treatment was interrupted due to fracture in 1.4% patients.

Promptly evaluate patients with signs or symptoms of potential fracture (e.g., pain, changes in mobility, deformity). There are no data on the effects of VITRAKVI on healing of known fractures or risk of future fractures.

Hepatotoxicity: Hepatotoxicity including drug induced liver injury (DILI) has occurred in patients taking VITRAKVI.

In patients who received VITRAKVI (n=444), increased AST of any grade occurred in 62% of patients and increased ALT of any grade occurred in 61%. Grade 3-4 increased AST or ALT occurred in 7% and 8% of patients, respectively. The median time to onset of increased AST was 1.9 months (range: 4 days to 3.8 years). The median time to onset of increased ALT was 1.9 months (range: 1 day to 4.9 years). Increased AST and ALT leading to dose modifications occurred in 1.6% and 3.2% of patients, respectively. Increased AST or ALT led to permanent discontinuation in 4 (0.9%) patients.

There have been reports from clinical studies and postmarketing cases of Grade ≥ 2 increases in ALT and/or AST with increases in bilirubin ≥ 2 x ULN.

Obtain liver function tests (ALT, AST, ALP and bilirubin) before initiation of VITRAKVI and monitor every 2 weeks during the first 2 months of treatment, then monthly thereafter, or more frequently following the occurrence of Grade 2 or greater AST or ALT elevation. Temporarily withhold, reduce the dose, or permanently discontinue VITRAKVI based on severity.

Embryo-Fetal Toxicity: VITRAKVI can cause fetal harm when administered to a pregnant woman. Larotrectinib resulted in malformations in rats and rabbits at maternal exposures that were approximately 11- and 0.7-times, respectively, those observed at the clinical dose of 100 mg twice daily. Advise women of the potential risk to a fetus. Advise females of reproductive potential to use an effective method of contraception during treatment and for 1 week after the last dose of VITRAKVI.
Adverse Reactions

The most common adverse reactions (≥20%), including laboratory abnormalities, were: increased AST (62%), increased ALT (61%), anemia (45%), hypoalbuminemia (44%), musculoskeletal pain (41%), increased alkaline phosphatase (40%), leukopenia (37%), lymphopenia (35%), neutropenia (34%), hypocalcemia (32%), fatigue (31%), vomiting (30%), cough (29%), constipation (27%), pyrexia (26%), diarrhea (26%), nausea (25%), abdominal pain (24%), dizziness (22%), and rash (21%).
Drug Interactions

Avoid coadministration of VITRAKVI with strong CYP3A4 inhibitors (including grapefruit or grapefruit juice), strong CYP3A4 inducers (including St. John’s wort), or sensitive CYP3A4 substrates. If coadministration of strong CYP3A4 inhibitors or inducers cannot be avoided, modify the VITRAKVI dose as recommended. If coadministration of sensitive CYP3A4 substrates cannot be avoided, monitor patients for increased adverse reactions of these drugs. For coadministration with moderate CYP3A4 inhibitors, monitor for adverse reactions more frequently and reduce the dosage based on severity. For coadministration with moderate CYP3A4 inducers, modify dose as recommended.
Use in Specific Populations

Lactation: Advise women not to breastfeed during treatment with VITRAKVI and for 1 week after the last dose.
Please see the full Prescribing Information for VITRAKVI (larotrectinib).

About TRK Fusion Cancer2

TRK fusion cancer occurs when an NTRK gene fuses with another unrelated gene, producing an altered TRK protein. The altered protein, or TRK fusion protein, becomes constitutively active or overexpressed, triggering a signaling cascade. These TRK fusion proteins act as oncogenic drivers promoting cell growth and survival, leading to TRK fusion cancer, regardless of where it originates in the body. TRK fusion cancer is not limited to certain types of tissues and can occur in any part of the body. TRK fusion is present in many tumors with varying frequency, including lung, thyroid, gastrointestinal cancers (colon, cholangiocarcinoma, pancreatic and appendiceal), sarcoma, CNS cancers (glioma and glioblastoma), salivary gland cancers (mammary analogue secretory carcinoma) and pediatric cancers (infantile fibrosarcoma and soft tissue sarcoma).2

TRK fusion cancer is diagnosed through the identification of NTRK gene fusions using specific tests, including those that employ next-generation sequencing (NGS) and fluorescence in situ hybridization (FISH).

IDEAYA Biosciences Announces Phase 1/2 Expansion for IDE397 and Trodelvy® Combination in MTAP-Deletion Urothelial Cancer

On April 10, 2025 IDEAYA Biosciences, Inc. (Nasdaq:IDYA), a precision medicine oncology company committed to the discovery and development of targeted therapeutics, reported the initiation of a Phase 1/2 expansion in the clinical trial evaluating IDE397, its investigational, potential first-in-class, small molecule methionine adenosyltransferase 2a (MAT2A) inhibitor, in combination with Gilead’s Trodelvy (sacituzumab govitecan-hziy), a Trop-2 directed antibody-drug conjugate (ADC), in methylthioadenosine phosphorylase (MTAP)-deletion urothelial cancer (UC) based on preliminary safety and clinical efficacy data (Press release, Ideaya Biosciences, APR 10, 2025, View Source [SID1234651877]).

IDE397 is a potent and selective small molecule inhibitor targeting (MAT2A), in patients having solid tumors with MTAP-deletion. The prevalence of MTAP-deletion is estimated to be approximately 26% in UC.

"We are pleased to advance the potential first-in-class clinical combination of IDE397 and Trodelvy into an initial Phase 1/2 expansion in MTAP-deletion UC based on preliminary safety and clinical efficacy observed. We are excited to continue to explore this novel combination given the high unmet medical need, as there are no approved therapies specifically for MTAP-deletion UC," said Darrin Beaupre, M.D., Ph.D., Chief Medical Officer, IDEAYA Biosciences.

Trodelvy is currently approved in more than 50 countries for second-line or later metastatic triple-negative breast cancer (TNBC) patients and in more than 40 countries for certain patients with pre-treated HR+/HER2- metastatic breast cancer. The use of Trodelvy in MTAP-deletion UC is investigational, and the safety and efficacy of this use have not been established.

A clinical program update on the IDE397 and Trodelvy combination is planned in 2025. In addition to the clinical trial program evaluating IDE397 in combination with Trodelvy, IDEAYA is has a monotherapy expansion study in MTAP-deletion NSCLC and UC and is expecting to initiate a wholly-owned clinical combination trial of IDE397 and IDE892, IDEAYA’s potential best-in-class, MTA-cooperative PRMT5 inhibitor in the second half of 2025.

Pursuant to the clinical study collaboration and supply agreement, IDEAYA and Gilead retain the commercial rights to their respective compounds, including with respect to use as a monotherapy or combination agent. IDEAYA is the study sponsor and Gilead will provide the supply of Trodelvy to IDEAYA.

IDE397 monotherapy or in combination with Trodelvy has not been approved by any regulatory agency and the efficacy and safety of this combination has not been established.

Trodelvy and Gilead are trademarks of Gilead Sciences, Inc., or its related companies.