On March 5, 2026 ITM Isotope Technologies Munich SE (ITM), a leading radiopharmaceutical biotech company, reported post-hoc subgroup analyses of the ITM-11 Phase 3 COMPETE trial in patients with Grade 1 or Grade 2 somatostatin receptor (SSTR)-positive gastroenteropancreatic neuroendocrine tumors (GEP-NETs). In patients with pancreatic neuroendocrine tumors (P-NETs), data showed that n.c.a. 177Lu-edotreotide (ITM-11) prolonged progression-free survival (PFS) and achieved higher objective response rates (ORR) when compared to everolimus. Data were presented by Thomas Walter, MD, PhD, professor of gastroenterology, Hospices Civil of Lyon, France, in a mini-oral presentation and in an accompanying poster at the 23rd Annual Meeting of the European Neuroendocrine Tumor Society (ENETS), held March 4-6, 2026 in Krakow, Poland.

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As previously announced at ENETS 2025, the COMPETE trial met its primary endpoint of PFS (23.9 vs. 14.1 months; p=0.022; HR 0.67, 95% CI [0.48, 0.95]). At ESMO (Free ESMO Whitepaper) 2025, ITM announced that COMPETE also met a key secondary endpoint of ORR (21.9% vs 4.2%, p<0.0001) in patients with GEP-NETs.

The COMPETE study enrolled a total of 309 GEP-NET patients, including 178 (57.6%) patients with P-NETs randomized 2:1 to either 177Lu-edotreotide (n=119) or everolimus (n=59). Of the 178 P-NET patients, 150 (84.3%) had non-functional tumors, meaning they did not produce hormones causing clinical symptoms, and 28 (15.7%) had functional tumors, in which excess hormone production can cause symptoms such as hypoglycemia (insulinoma), or diarrhea and peptic ulcer (Zollinger Elison syndrome).

Key findings in the P-NETs population showed:

Median PFS was longer in the 177Lu-edotreotide arm compared to everolimus (24.5 months vs. 14.7 months; p=0.114; HR 0.70, 95% CI [0.45, 1.09]) and ORR in the 177Lu-edotreotide arm was 33.3% vs. 3.6% in everolimus arm.
ORR in the 177Lu-edotreotide arm was ≥ 30% in P-NET patients with non-functional disease, across all patients regardless of line of therapy and Ki-67 index. This includes 38.1% ORR in P-NET patients with non-functional disease and 34.2% ORR in patients with a Ki-67 index ≥10%.
Median overall survival was numerically longer in the 177Lu-edotreotide arm compared to everolimus (65.7 months vs. 49.3 months) at the time of analyses; data continue to mature with ongoing five-year follow up.
The overall safety profile in P-NET patients receiving 177Lu-edotreotide compared to everolimus was similar or potentially improved, and included fewer serious adverse events (SAEs) (29.1% vs. 43.1%). Lower incidence of adverse events suspected to be related to the study drug was seen in the 177Lu-edotreotide arm vs. everolimus arm (83.8% vs. 96.6%).
"Given that the data on peptide receptor radionuclide therapy in pancreatic NETs has been limited to date, we are encouraged by the activity of 177Lu-edotreotide observed in this prespecified exploratory subgroup of patients with Grade 1 or 2 pancreatic NETs, who represented approximately 58% of trial participants," said Thomas Walter, MD, PhD, professor of gastroenterology, Hospices Civil of Lyon, France.

"These additional results from our Phase 3 COMPETE trial provide important insights into treatment options for patients with pancreatic NETs, and further enhance the robust clinical data of 177Lu-edotreotide," said Dr. Celine Wilke, chief medical officer of ITM.

177Lu-edotreotide (ITM-11) is an investigational product pending review by the U.S. Food and Drug Administration (FDA) and is not approved by any regulatory authority for the safety and/or efficacy of any intended use.

ENETS Oral Presentation Details
Title: 177Lu-edotreotide for the Treatment of Pancreatic Neuroendocrine Tumours: A Subgroup Analysis from the COMPETE Study
Date and Time: March 5, 2026, 11:00 am-12:30 pm CET Session; 11:50-11:57 am CET Oral Presentation
Session and Room Number: Clinical Science, Session 2B: Abstract session; Theatre Hall (S2)
Presenter: Thomas Walter, PhD, MD, Professor of Gastroenterology, Hospices Civil of Lyon, France

The e-poster will be accessible to registered participants during the event and available on www.enets.org after the conference.

About the COMPETE Trial
The COMPETE trial (NCT03049189) evaluated 177Lu-edotreotide (ITM-11), a proprietary, synthetic, targeted radiotherapeutic investigational agent compared to everolimus, a targeted molecular standard-of-care therapy, in patients with inoperable, progressive Grade 1 or Grade 2 gastroenteropancreatic neuroendocrine tumors (GEP-NETs). This trial met its primary endpoint, with 177Lu-edotreotide demonstrating clinically and statistically significant improvement in progression-free survival (PFS) compared to everolimus. 177Lu-edotreotide is also being evaluated in COMPOSE, a Phase 3 study in patients with well-differentiated, aggressive Grade 2 or Grade 3, SSTR-positive GEP-NET tumors.

(Press release, ITM Isotopen Technologien Munchen, MAR 5, 2026, View Source [SID1234663322])

On March 5, 2026 Atavistik Bio, a biotechnology company discovering the next generation of selective allosteric therapeutics, reported the closing of a $40 million extension to its Series B financing from new investor RA Capital Management, bringing the total round proceeds to $160 million. RA Capital joins other top-tier investors who participated in the Series B round, including Nextech Invest, The Column Group, Lux Capital and Regeneron Ventures, as previously announced in December 2025. Atavistik Bio will use the proceeds from the upsized Series B financing to fund clinical development of ATV-1601, a potential best-in-class AKT1-selective oral inhibitor for HHT, and its JAK2 V617F mutant-selective inhibitor program for MPNs through clinical proof of concept.

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"We’re excited to welcome RA Capital as an investor in Atavistik Bio. Our Series B round, backed by a highly respected syndicate, reflects strong belief in our selective allosteric programs and our focus to advance meaningful therapies for patients with severe diseases," said Bryan Stuart, Chief Executive Officer at Atavistik Bio. "This additional funding further strengthens our ability to accelerate the development of best-in-class therapies designed to deliver superior efficacy, improved tolerability profiles, and potentially transformative outcomes for patients."

"We are pleased to support Atavistik Bio in this next phase of growth as the company is at the forefront of developing transformative therapies for HHT and MPNs," said Nandita Shangari, PhD, Managing Director at RA Capital Management. "Atavistik Bio’s highly experienced team and a pipeline of high-quality programs targeting significant unmet need, position the company to create meaningful value."

About Hereditary Hemorrhagic Telangiectasia (HHT), AKT1 Inhibition and ATV-1601

HHT is a severe inherited bleeding disorder that affects more than 1.6 million people globally, with no approved therapies currently available. This condition often leads to frequent bleeding episodes and vascular shunts, resulting in chronic anemia, multiorgan damage, and life-threatening complications. AKT1 hyperactivation is a hallmark of HHT and has been shown to drive the vascular pathology of HHT. Selectively inhibiting AKT1, the primary AKT isoform and driver of abnormal endothelial growth implicated in HHT, offers a novel and potentially disease-modifying therapeutic approach for this difficult disease. Although there has been substantial investment in pan-AKT inhibitors, their use is limited by AKT2-driven toxicities, most notably hyperglycemia, which impact tolerability and restrict their use for chronic dosing. ATV-1601 is an oral allosteric inhibitor that selectively inhibits AKT1.

ATV-1601 was evaluated in a Phase 1 oncology study, and demonstrated a favorable safety profile, validating its differentiated selectivity profile that addresses key limitations of pan-AKT inhibitors. Development efforts will now focus on advancing ATV-1601 in HHT.

About Myeloproliferative Neoplasms (MPNs) and Selective Targeting of the JAK2 V617F Mutation

MPNs are a group of rare chronic blood cancers for which current treatment options are limited. The JAK2 V617F mutation is the most common driver mutation in patients living with MPNs, affecting approximately 95% of patients with polycythemia vera, 60% of patients with essential thrombocythemia, and 55% of patients with myelofibrosis. Approved pan-JAK inhibitors, such as ruxolitinib, provide symptom relief, but non-selectively inhibit both mutant and wild-type JAK2. This limits the ability to reduce JAK2 V617F mutant allele burden and can disrupt normal blood cell production regulated by wild-type JAK2, contributing to adverse events and treatment discontinuation. Selectively targeting the JAK2 V617F mutation has the potential to reduce mutant allele burden, preserve normal bone marrow function, and have a disease modifying impact that will substantially improve long term outcomes for patients with MPNs.

(Press release, Atavistik Bio, MAR 5, 2026, View Source [SID1234663321])

On March 5, 2026 Erasca, Inc. (Nasdaq: ERAS), a clinical-stage precision oncology company singularly focused on discovering, developing, and commercializing therapies for patients with RAS/MAPK pathway-driven cancers, reported a clinical trial collaboration and supply agreement (CTCSA) with Tango Therapeutics, Inc. (Nasdaq: TNGX; "Tango") to evaluate Erasca’s pan-RAS molecular glue, ERAS-0015, with Tango’s PRMT5 inhibitor, vopimetostat (TNG462).

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"We’ve disclosed encouraging early clinical activity for our potential best-in-class molecular glue, ERAS-0015, including first clinical responses in multiple patients with differing tumor types and RAS mutations at just 1/10th of the dose at which first clinical responses were observed with RMC-6236," said Jonathan E. Lim, M.D., Erasca’s chairman, CEO, and co-founder. "Combining ERAS-0015 with Tango’s potentially first-in-class PRMT5 inhibitor represents a promising opportunity to redefine the standard of care in patients with MTAP-deleted RAS-mutant (MTAPdel RASm) cancers, where treatment options remain limited. We are excited to partner with Tango to evaluate this approach in these patients with high unmet needs."

This agreement will support a Phase 1/2 clinical trial evaluating ERAS-0015 in combination with vopimetostat in patients with MTAPdel pancreatic or MTAPdel RASm non-small cell lung cancer (NSCLC). Erasca will supply ERAS-0015 free of charge, and Tango will be the trial sponsor. Each company will retain commercial rights to their respective compound, and the agreement is mutually non-exclusive.

Nearly all MTAP-deleted pancreatic cancers and 30% of MTAP-deleted NSCLC tumors harbor co-occurring RAS mutations, creating a dependency that makes these cancer cells particularly susceptible to simultaneous RAS and PRMT5 inhibition. Combining a pan-RAS molecular glue with a PRMT5 inhibitor may provide a differentiated, dual-targeted approach designed to shut down the RAS signaling pathway and more strongly suppress PRMT5 in MTAP-deleted tumor cells, potentially leading to deeper and more durable responses and reducing the likelihood of resistance in these difficult-to-treat cancers.

About ERAS-0015
ERAS-0015 is an oral, highly potent pan-RAS molecular glue designed to inhibit RAS signaling with a potential best-in-class profile. Erasca is evaluating ERAS-0015 in the AURORAS-1 Phase 1 trial in patients with RAS-mutant solid tumors. Early dose escalation data in AURORAS-1 demonstrated favorable safety and tolerability, well-behaved, linear PK, and confirmed and unconfirmed responses in multiple patients across multiple tumor types with different RAS mutations, including confirmed and unconfirmed partial responses at doses as low as 8 mg once daily (QD). In preclinical studies versus RMC-6236, ERAS-0015 demonstrated approximately 8-21 times higher binding affinity to cyclophilin A (CypA) , approximately 5 times greater potency in RAS inhibition, and greater in vivo antitumor activity evidenced by achieving comparable or greater tumor growth inhibition or regression at doses that are as low as approximately one-tenth to one-fifth of the dose of RMC-6236. ERAS-0015 is also designed to prevent resistance against mutant-selective inhibitors through inhibition of RAS wildtype variants. In addition, ERAS-0015 has demonstrated favorable absorption, distribution, metabolism, and excretion (ADME) and pharmacokinetic (PK) properties in multiple animal species.

(Press release, Erasca, MAR 5, 2026, View Source [SID1234663320])

On March 5, 2026 Kestrel Therapeutics Inc. ("Kestrel" or the "Company"), a clinical stage biotechnology company developing next-generation small-molecule inhibitors targeting mutant KRAS, reported that the U.S. Food and Drug Administration (FDA) has cleared its Investigational New Drug (IND) application for KST-6051, an investigational, oral, small-molecule inhibitor designed to target KRAS.

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Kestrel is advancing KST-6051 into the clinic and expects to initiate a first-in-human Phase 1 dose-escalation clinical trial FALCON by the end of the first quarter. The trial, designed to evaluate safety, tolerability and preliminary anti-tumor activity, will enroll patients with advanced or metastatic KRAS-mutant solid tumors, including pancreatic ductal adenocarcinoma (PDAC), colorectal cancer (CRC), non-small cell lung cancer (NSCLC), and others.

"IND approval for KST-6051 is a significant milestone for Kestrel and an important step forward for patients with KRAS-driven cancers," said Dr. Frank G. Haluska, President and Chief Executive Officer of Kestrel Therapeutics. "KST-6051 represents our next-generation approach to pan-KRAS inhibition, leveraging proprietary and unique Switch-II pocket chemistry to target KRAS in both the ON- and OFF-states. We are excited to initiate our first study as we work toward initial clinical readouts anticipated in late 2026."

About KST-6051

KST-6051 is a potential best-in-class, oral pan-KRAS inhibitor, developed for the treatment of KRAS-driven cancers. KST-6051 is a potent and selective inhibitor of KRAS with activity against KRAS in both its active (GTP-bound) and inactive (GDP-bound) states. Preclinical data demonstrate robust on-target pathway modulation, anti-proliferative activity, and efficacy at well-tolerated doses in multiple human KRAS mutant tumor models. The Company is initiating a Phase 1 study in patients with KRAS-mutant advanced/metastatic solid tumors. Its clinical development will ultimately address pancreatic ductal adenocarcinoma (PDAC), colorectal cancer (CRC), non-small cell lung cancer (NSCLC), and other KRAS-driven malignancies.

(Press release, Kestrel Therapeutics, MAR 5, 2026, View Source [SID1234663319])

On March 5, 2026 Hopewell Therapeutics, Inc., a Boston-based next-generation lipid nanoparticle (LNP) company ("Hopewell"), reported that it entered into a sublicense agreement with Foxcroft Therapeutics, Inc., the developer of novel cancer vaccines ("Foxcroft"), granting Foxcroft a global sublicense to certain of its tissue-targeting LNPs (ttLNPs). Hopewell and Foxcroft will collaborate on their evaluation of Hopewell’s ttLNPs as potential delivery vehicles for Foxcroft’s cancer vaccines.

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Hopewell is currently developing ttLNPs as a delivery vehicle for a broad range of clinical and therapeutic applications, including vaccines, gene therapies, immune-oncology, and pulmonary therapies, targeting tissues in the lung, brain, bone marrow, ovaries, spleen, lymph nodes, kidneys, liver, and other vital organs. Pre-clinical testing has demonstrated Hopewell ttLNPs to perform more effectively than other LNPs available in the market.

In February 2025, Dr. Qiaobing Xu, Founder and President of Hopewell, authored a paper entitled "Antitumour vaccination via the targeted proteolysis of antigens isolated from tumour lysates," which described a novel tumor lysate-based cancer vaccine, delivered through LNPs that target the lymph nodes.1

In September 2025, Foxcroft obtained from Tufts University the exclusive global license to this cancer vaccine technology. The present Hopewell sublicense gives Foxcroft access to multiple ttLNPs as candidate delivery vehicles for its vaccine. Foxcroft plans to conduct confirmatory testing of vaccine formulations in large mammal trials, starting with a canine clinical trial expected to commence later this year.

The Hopewell sublicense includes a significant, non-refundable, up-front license fee to Hopewell, royalties on net sales, regulatory milestone payments, and up to $100 million of sales-based milestone payments.

"Hopewell is thrilled to announce the first sublicense of its ttLNP technology in the exciting field of cancer vaccines," commented Dr. Xu. "We look forward to supporting Foxcroft to bring this important anti-cancer therapy to human testing as quickly as possible."

Foxcroft’s management stated, "We recognize that Hopewell’s LNP library provides superior targeted delivery solutions for a number of clinical and therapeutic applications, including our vaccine. Over the months ahead, we are excited to work further with the Hopewell team to further evaluate the sublicensed LNPs."

(Press release, Hopewell Therapeutics, MAR 5, 2026, View Source [SID1234663318])