On July 2, 2026 Elicio Therapeutics, Inc. (Nasdaq: ELTX) ("Elicio" or the "Company"), a clinical-stage biotechnology company developing next-generation immunotherapies for KRAS-driven cancers, reported that it has entered into a definitive securities purchase agreement led by two new fundamental institutional investors with participation from a large existing shareholder for the purchase of an aggregate of 4,380,313 shares of its common stock pursuant to a registered direct offering (the "Offering"). The Offering is expected to result in gross proceeds of approximately $15 million, before deducting placement agents’ fees and other Offering expenses. The closing of the Offering is expected to occur on or about July 6, 2026, subject to the satisfaction of customary closing conditions. Elicio intends to use the net proceeds from the Offering, together with its existing cash, cash equivalents and marketable securities, to primarily fund the planned Phase 1 clinical development of ELI-002 7P in metastatic PDAC and Elicio’s pipeline and platform, as well as for working capital and general corporate purposes.

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Titan Partners, a division of American Capital Partners, is acting as lead placement agent for the Offering. B. Riley Securities, Inc. is acting as co-placement agent for the Offering.

The Offering is being made pursuant to a shelf registration statement on Form S-3 (File No. 333-293861) initially filed with the Securities and Exchange Commission ("SEC") on February 27, 2026, as amended on March 12, 2026, and declared effective by the SEC on March 16, 2026 (the "Registration Statement"). The shares of common stock are being offered only by means of a prospectus, including a prospectus supplement, forming a part of the effective registration statement. The prospectus supplement and the accompanying prospectus relating to, and describing the terms of, the Offering will be filed with the SEC and will be available for free on the SEC’s website at www.sec.gov. Electronic copies of the prospectus supplement and accompanying prospectus may also be obtained, when available, by contacting Titan Partners Group LLC, a division of American Capital Partners, LLC, 4 World Trade Center, 49th Floor, New York, NY 10007, by phone at (929) 833-1246 or by email at [email protected], or B. Riley Securities, Inc. at 1655 Fort Myer Drive, Suite 1200, Arlington, Virginia 22209, Attention: Syndicate Prospectus Department, by telephone at 703-312-9580 or by email at [email protected].

This press release shall not constitute an offer to sell or a solicitation of an offer to buy any of the securities, nor shall there be any sale of these securities in any state or other jurisdiction in which such offer, solicitation or sale would be unlawful prior to the registration or qualification under the securities laws of any such state or other jurisdiction.

About ELI-002

Elicio’s lead product candidate, ELI-002, is a structurally novel investigational AMP cancer immunotherapy that targets cancers that are driven by mutations in the KRAS-gene—a prevalent driver of many human cancers. ELI-002 is comprised of two powerful components that are built with Elicio’s proprietary AMP technology consisting of AMP-modified mutant KRAS peptide antigens and ELI-004, an AMP-modified CpG oligodeoxynucleotide adjuvant that is available as an off-the-shelf subcutaneous administration.

ELI-002 7P (7-peptide formulation) was evaluated in the randomized Phase 2 AMPLIFY-7P trial in patients with mKRAS-driven pancreatic cancer (NCT05726864). The Phase 2 AMPLIFY-7P trial included patients with mKRAS-positive pancreatic cancer who completed standard therapy but remain at high risk of relapse. Based on topline results and post-hoc analyses, Elicio has refined its Phase 3 development strategy to focus on patients with lower residual disease burden and extended treatment duration. Elicio intends to initiate a Phase 1 study in metastatic PDAC designed to provide a rapid assessment of clinical activity through a focused, confirmatory study, subject to funding. Elicio plans to use the study findings to further evaluate checkpoint inhibitor combinations and help inform future development strategies in metastatic PDAC and the adjuvant PDAC Phase 3 trial. At the time of the Phase 2 AMPLIFY-7P analysis, data for overall survival remained immature. The ELI-002 7P formulation is designed to provide immune response coverage against seven of the most common KRAS mutations present in 25% of all solid tumors, thereby increasing the potential patient population for ELI-002.

(Press release, Elicio Therapeutics, JUL 2, 2026, View Source [SID1234669060])

On July 2, 2026 Treos Bio, a clinical-stage biotechnology company developing off-the-shelf and personalized active cancer immunotherapies based on its proprietary PEPI Technology, reported new translational data from the Phase Ib/II OBERTO-301 study (NCT05243862), presented at the ESMO (Free ESMO Whitepaper) Gastrointestinal Cancers Congress 2026.

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Conducted in collaboration with Mayo Clinic, the retrospective translational analysis demonstrates that PolyPEPI1018 treatment in combination with anti-PD-L1 immunotherapy induced measurable immune remodeling in patients with microsatellite-stable metastatic colorectal cancer (MSS mCRC), a tumor type generally considered resistant to checkpoint inhibition.

The retrospective analysis evaluated paired baseline and on-treatment tumor biopsies and peripheral blood samples from OBERTO-301 patients treated with PolyPEPI1018 plus atezolizumab. Post-treatment tumor samples showed increased CD8+ T-cell density and PD-L1 expression, indicating conversion toward a more inflamed tumor microenvironment.
T-cell receptor (TCR) sequencing demonstrated selective expansion of tumor-reactive T-cell clonotypes, including TCRs directed against PolyPEPI1018 antigens, additional tumor-associated antigens and neoantigens. The analysis also suggested treatment-induced antigen spreading beyond the PolyPEPI1018-targeted epitopes.

Importantly, higher numbers of tumor-reactive TCR clonotypes and higher post-treatment CD8+ TIL density were associated with improved clinical outcomes, including longer overall survival and progression-free survival. Together, these findings provide mechanistic evidence that therapeutic vaccination targeting shared tumor-associated antigens can remodel the immune microenvironment of MSS colorectal cancer converting immunologically "cold" tumors into a more immunologically active, potentially checkpoint-responsive tumor microenvironment.

"MSS colorectal cancer has long been one of the most difficult settings for immunotherapy because these tumors typically lack the immune activity needed for checkpoint inhibitors to work," said Dr. Eniko Toke, Co-founder and Chief Scientific Officer of Treos Bio. "What is encouraging in this analysis is not only that we observed immune activation in the tumor microenvironment, but that the depth of that response was associated with patient outcomes. Together with our recent clinical and platform data, these findings strengthen the rationale for advancing PolyPEPI1018 combinations in MSS colorectal cancer and applying PEPI Technology across other difficult-to-treat tumors."

Poster number: 115P
Presentation: 02 July 2026
Congress: ESMO (Free ESMO Whitepaper) Gastrointestinal Cancers Congress 2026

(Press release, Treos Bio, JUL 2, 2026, View Source [SID1234669059])

On July 2, 2026 VERAXA Biotech AG (NASDAQ: VRXA; "VERAXA"), an emerging leader in designing novel cancer therapies, reported the initiation of cell line development for its lead BiTAC T-cell engager (BiTAC-TCE) program. VERAXA has engaged ATUM, a global leader in bioengineering and cell line development, to apply the proprietary Leap-In Transposase technology to support stable clonal cell line generation. The collaboration marks a key step in progressing VERAXA’s most advanced T-cell engager candidate toward IND/CTA-enabling activities and supports future clinical development.

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"Today’s news underscores our commitment to accelerate the development path of our growing BiTAC-TCE portfolio. Initiating cell line development with ATUM is an important next step for our lead BiTAC-TCE program following the encouraging preclinical data we presented at AACR (Free AACR Whitepaper)," said Christoph Erkel, Ph.D., Vice President Research & Development of VERAXA. "Working with a recognized cell line development partner like ATUM allows us to pair our differentiated molecular design with expertise and workflows built for exactly this kind of advanced multi-chain formats."

Cell line development is an important milestone in translating a therapeutic candidate into a manufacturable product. The collaboration with ATUM is intended to support the generation of stable and high-producing clonal cell lines that will be used throughout CMC development, including early process, analytical, and formulation development, as well as the supply of material for nonclinical studies. ATUM’s Leap-In Transposase technology is designed to support efficient stable cell line generation and is particularly relevant for multi-chain antibody formats where balanced expression of multiple components is important, such as VERAXA’s BiTAC-TCEs. ATUM‘s Leap-In Transposase technology has supported the generation of stable cell lines used in over 50 IND submissions, providing VERAXA with an established cell line development approach for advanced biologic formats.

A new generation of T-cell engagers

T-cell-engaging bispecific molecules redirect cytotoxic T-cells to eliminate cancer cells, typically by binding the CD3 receptor on T-cells while simultaneously engaging a target protein on the tumor. While effective in select indications, conventional TCEs remain limited by toxicity; because their tumor target is often also present on healthy tissue, on-target but off-tumor T-cell activation can drive serious side effects and narrow the therapeutic window. A large proportion of conventional bispecific TCEs fail in development for this reason.

VERAXA’s BiTAC-TCE approach is designed to address this challenge at its source. Rather than delivering a single, fully active molecule, the BiTAC strategy splits the T-cell engager into two complementary precursors. In their isolated form, each precursor retains its tumor-binding capability while the CD3-binding function remains inactivated. Only when both precursors bind their respective targets on the same cell is the CD3-binding domain reconstituted and activated. This "AND"-gated mechanism restricts T-cell activity to cells displaying both tumor markers, sparing healthy cells that carry only one.

A dual-target, conditional-activation design distinguishes BiTAC-TCEs from both traditional TCEs and from masked-TCE approaches that rely on a single antibody whose effector function is shielded until cleaved in the tumor microenvironment. By requiring the simultaneous engagement of two distinct antigens to assemble the active engager, BiTAC-TCEs are engineered for greater tumor selectivity, with the goal of enabling higher dosing and a meaningfully wider therapeutic window.

Initial data from VERAXA’s most advanced BiTAC-TCE program were presented at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026, in April. In those studies, VERAXA’s BiTAC-TCE candidate performed as intended in vitro and in vivo, attacking cancer cells displaying both target molecules while sparing cells expressing only one of the two targets. The data demonstrated a superior safety profile with matching efficacy compared with a more traditional TCE, pointing to the possibility of a meaningfully improved therapeutic index. The related posters are available on the VERAXA website at www.veraxa.com.

(Press release, Veraxa Biotech, JUL 2, 2026, View Source [SID1234669058])

On July 2, 2026 Revolution Medicines, Inc. (Nasdaq: RVMD), a late-stage clinical oncology company developing targeted therapies for patients with RAS-addicted cancers, reported results from two Phase 1/2 clinical trials evaluating zoldonrasib, its oral RAS(ON) G12D-selective covalent inhibitor, in combination regimens for patients with RAS G12D metastatic pancreatic ductal adenocarcinoma (PDAC). The results, which will be presented today in a proffered paper session at the 2026 European Society for Medical Oncology (ESMO) (Free ESMO Whitepaper) Gastrointestinal Cancers Congress, include zoldonrasib in combination with standard of care chemotherapy in previously untreated patients and zoldonrasib in combination with daraxonrasib, the company’s oral RAS(ON) multi-selective inhibitor, in previously treated patients.

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"The Phase 3 RASolute 302 results provided clinical validation of RAS(ON) inhibition with daraxonrasib in second line metastatic pancreatic cancer and established a strong foundation for evaluating this therapeutic approach across additional RAS genotypes, treatment settings and combination strategies. The results presented at ESMO (Free ESMO Whitepaper) GI demonstrate compelling proof-of-concept for two zoldonrasib-based regimens in RAS G12D disease: combination with standard of care chemotherapy in previously untreated patients and a RAS(ON) inhibitor doublet with daraxonrasib in previously treated patients. Together, these findings are the foundation of two distinct Phase 3 strategies we are pursuing in previously untreated metastatic RAS G12D pancreatic cancer: the ongoing RASolute 305 trial evaluating zoldonrasib plus standard of care chemotherapy, and the planned RASolute 309 trial evaluating the combination of zoldonrasib plus daraxonrasib," said Alan Sandler, M.D., chief development officer of Revolution Medicines.

Safety and Efficacy of Zoldonrasib Plus Chemotherapy in Patients with First Line RAS G12D Metastatic Pancreatic Cancer (Abstract #340O)

RMC-GI-102 (NCT06445062) is an ongoing Phase 1/2 trial evaluating zoldonrasib 1200 mg once daily in combination with investigator’s choice of standard of care chemotherapy in patients with previously untreated metastatic RAS G12D PDAC. Investigator’s choice of chemotherapy includes modified FOLFIRINOX (mFFX) or gemcitabine plus nab-paclitaxel (GnP). As of the February 8, 2026 data cutoff, the trial enrolled 41 patients in the zoldonrasib plus mFFX arm and 40 patients in the zoldonrasib plus GnP arm.

Zoldonrasib demonstrated a manageable safety and tolerability profile in combination with standard chemotherapy. The safety profile of zoldonrasib in combination with chemotherapy was broadly consistent with the established profiles of each respective chemotherapy regimen. Grade 3 or greater treatment-related adverse events (TRAEs) occurred in 61% of patients who received the zoldonrasib plus mFFX and 80% of patients who received zoldonrasib plus GnP. The most common Grade 3 or greater TRAEs with zoldonrasib plus mFFX were decreased neutrophil count (37%), anemia (12%), and platelet count decreased (7%). The most common Grade 3 or greater TRAEs with zoldonrasib plus GnP were decreased neutrophil count (35%), anemia (28%), and fatigue (25%). No Grade 5 TRAEs were reported in either arm. The mean dose intensity was 86% with zoldonrasib plus mFFX and 90% with the zoldonrasib plus GnP.

In the trial, zoldonrasib with chemotherapy showed compelling antitumor activity, with an objective response rate (ORR) of 82% (95% confidence interval [CI]: 60, 95) and disease control rate (DCR) of 96% (95% CI: 77, 100) in the mFFX population, and an ORR of 61% (95% CI: 42, 78) and DCR of 90% (95% CI: 74, 98) in the GnP population.

These preliminary safety and clinical activity data support the ongoing RASolute 305 pivotal trial (NCT07621718), a global, randomized, double-blind placebo-controlled Phase 3 clinical trial evaluating zoldonrasib plus investigator’s choice of standard of care chemotherapy compared with placebo plus investigator’s choice of chemotherapy in patients with previously untreated metastatic RAS G12D PDAC.

Safety and Efficacy of Zoldonrasib Plus Daraxonrasib in Patients with Second Line-Plus RAS G12D Metastatic Pancreatic Cancer (Abstract #341O)

RMC-9805-001 (NCT06040541) is a Phase 1 trial evaluating zoldonrasib 1200 mg once daily plus daraxonrasib 300 mg once daily in advanced solid tumors with RAS G12D mutations. As of the February 9, 2026 data cutoff, 60 patients with RAS G12D metastatic PDAC who had previously received one or more prior lines of therapy were treated with the combination.

Zoldonrasib plus daraxonrasib demonstrated a manageable safety and tolerability profile that was broadly consistent with the established profile of daraxonrasib monotherapy. Grade 3 or greater TRAEs occurred in 35% of patients who received the combination. Among TRAEs occurring in 10% or more of all patients, the most common Grade 3 or greater events were rash (12%), anemia (10%), and stomatitis/mucositis (7%). Few patients discontinued due to TRAES; 2% discontinued zoldonrasib and 5% discontinued daraxonrasib. The mean dose intensity was 88% for zoldonrasib and 76% for daraxonrasib.

The zoldonrasib plus daraxonrasib combination demonstrated compelling antitumor activity in patients with previously treated metastatic PDAC. In the second line cohort (2L) (N=30), the ORR was 50% (95% CI: 31–69) and DCR was 97% (95% CI: 83–100). Median progression-free survival (PFS) in the 2L cohort was 9.6 months (95% CI: 7.1–NE), with a 6-month PFS rate of 71%. Median overall survival (OS) in the 2L cohort was not yet estimable, with a 6-month OS rate of 89%. In the third line and beyond (3L+) cohort (N=30), the ORR was 47% (95% CI: 28–66) and DCR was 90% (95% CI: 74–98). Median PFS in the 3L+ cohort was 7.6 months (95% CI: 4.6–10.5), with a 6-month PFS rate of 59%. Median OS in the 3L+ cohort was 10.5 months (95% CI: 6.7–NE), with a 6-month OS rate of 82%.

These safety and clinical activity data support the planned pivotal global, Phase 3 RASolute 309 clinical trial of zoldonrasib plus daraxonrasib versus GnP in patients with previously untreated RAS G12D metastatic PDAC.

About Pancreatic Cancer and Pancreatic Ductal Adenocarcinoma
Pancreatic cancer is one of the most lethal malignancies, characterized by its typically late-stage diagnosis, resistance to standard chemotherapy, and high mortality rate. Pancreatic ductal adenocarcinoma, or PDAC, is the most common form of pancreatic cancer. Due to the lack of early symptoms and effective detection methods, approximately 80% of patients are diagnosed with advanced or metastatic disease. PDAC is the most commonly RAS-driven malignancy of all major cancers, with more than 90% of patients having tumors that harbor RAS mutations.1 RAS G12D is the most prevalent RAS mutation subtype in PDAC, occurring in 40% of patients, and has been associated with poorer outcomes than RAS wild-type disease and certain other RAS-mutant subgroups.1-4

About Zoldonrasib
Zoldonrasib is an investigational, oral RAS(ON) G12D-selective covalent tri-complex inhibitor. RAS G12D is the most prevalent RAS mutation, accounting for 29% of all RAS cancers.1 Across tumor types, approximately 61,000 new patients with RAS G12D cancers are estimated each year in the U.S., and no targeted therapy is currently approved for these patients.5 Zoldonrasib is currently being evaluated as a monotherapy and in combination with other therapies, including with Revolution Medicines’ RAS(ON) multi-selective inhibitor daraxonrasib (RMC-6236), as well as standard of care regimens in lung and gastrointestinal cancers.

About Daraxonrasib
Daraxonrasib is an investigational, oral RAS(ON) multi-selective, non-covalent tri-complex inhibitor. The U.S. Food and Drug Administration (FDA) granted daraxonrasib Breakthrough Therapy Designation and Orphan Drug Designation for the treatment of patients with previously treated metastatic pancreatic ductal adenocarcinoma (PDAC) harboring G12 mutations. In addition, daraxonrasib was selected for the FDA Commissioner’s National Priority Voucher pilot program, which is intended to accelerate the development and review of therapies aligned with U.S. national health priorities.

Daraxonrasib is designed to target cancers driven by a broad range of common RAS genotypes, including PDAC, non-small cell lung cancer (NSCLC), and colorectal cancer. Daraxonrasib is being advanced through a global Phase 3 registrational program comprising four trials, including the completed RASolute 302 trial and three additional trials in patients with PDAC and metastatic RAS mutant NSCLC.

(Press release, Revolution Medicines, JUL 2, 2026, View Source [SID1234669057])

On July 2, 2026 OnKure Therapeutics, Inc. (Nasdaq: OKUR), a clinical-stage biopharmaceutical company focused on developing novel precision medicines, reported that it will host a virtual key opinion leader (KOL) event on Wednesday, July 15, 2026 at 11:00 AM ET featuring Benjamin F. Cravatt, PhD (The Scripps Research Institute) and Robert Abraham, PhD (Engine Biosciences). They will join company management to discuss the significance of PI3Kα selectivity and the Company’s structure-based drug design approach for discovering allosteric pan-mutant PI3Kα inhibitors. To register, click here.

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Management will provide an overview of OnKure’s strategy for designing its portfolio of next-generation pan-mutant PI3Kα inhibitors.

A live question and answer session will follow the formal presentations.

About Benjamin F. Cravatt, PhD
Benjamin F. Cravatt, PhD, is Professor and Norton B. Gilula Chair of Chemical Biology in the Department of Chemistry at The Scripps Research Institute. His research group has developed several innovative chemical technologies that enable and expand protein and drug discovery on a global scale. Further application of these methods has offered insights to biological pathways that play important roles in human physiology and disease. Dr. Cravatt obtained his undergraduate education at Stanford University, receiving a B.S. in the Biological Sciences and a B.A. in History. He then received a Ph.D. from The Scripps Research Institute (TSRI) in 1996. Professor Cravatt joined the faculty at TSRI in 1997. Dr. Cravatt is co-founder of several biotechnology companies, including Activx Biosciences, Abide Therapeutics, Vividion Therapeutics, and Belharra Therapeutics. Dr. Cravatt’s honors include a Searle Scholar Award, the Eli Lilly Award in Biological Chemistry, the ASBMB Merck Award, the Wolf Prize in Chemistry, the Heinrich Wieland Prize, the Tetrahedron Award for Creativity in Bioorganic and Medicinal Chemistry, The NAS Award in Chemical Science, and memberships in the National Academies of Inventors, Medicine, and Sciences.

About Robert Abraham, PhD
Robert Abraham, PhD, currently serves as the Chief Scientific Officer at Engine Biosciences. He has previously held leadership roles in several successful biotechnology companies, including Odyssey Therapeutics and Vividion Therapeutics. Prior to entering the biotech sector, Bob was Chief Scientific Officer of the Oncology R&D Group at Pfizer, where he led teams that delivered multiple clinical candidates and 11 FDA-approved oncology drugs. One of those clinical candidates, gedatolisib, is a pan-PI3K/mTOR inhibitor, which has recently delivered highly promising clinical data in ER+ HER2- breast cancer patients. Before joining the pharmaceutical industry, Bob was a prolific immunology and pharmacology researcher with over 230 scientific publications while at Sanford-Burnham-Prebys Medical Research Institute, Duke University Medical Center, and the Mayo Clinic. His research accomplishments included the molecular cloning and functional characterization of the key PI3K pathway component, mTOR. He is also a member of the scientific advisory boards of several public and private companies, and a retained scientific advisor for Google Ventures.

About Next-Generation PI3Kα Pan-Mutant Programs

OnKure is advancing a portfolio that includes two next-generation PI3Kα pan-mutant inhibitor programs, OKI-345 for breast cancer and OKI-355 for vascular anomalies. These candidates are designed to selectively inhibit mutant PI3Kα while sparing wildtype PI3Kα, with the potential to deliver a wider therapeutic index while avoiding class-limiting toxicities associated with first-generation PI3Kα inhibitors. By providing high and sustained target coverage across all hotspot PI3Kα mutations, these programs are designed to support the potential for deep and durable responses as both monotherapy and in combination regimens. In addition, the Company’s pan-mutant candidates are designed to have minimal drug-drug interaction potential, supporting broad combinability with current standards of care. Together with a commanding intellectual property estate, OnKure believes it is well positioned to address a significant unmet need across various PI3Kα-driven indications.

PI3Kα mutations represent the most common driver alterations in key subtypes of vascular anomalies, where PIK3CA variants lead to dysregulated signaling that promotes abnormal cell growth, proliferation, and survival. OnKure believes that OKI-355 has significant potential to address this large and underserved patient population as a differentiated systemic chronic therapy.

OnKure plans to submit an Investigational New Drug (IND) application to the U.S. Food and Drug Administration (FDA) for each of OKI‑345 and OKI‑355 in the first half of 2027.

(Press release, OnKure Therapeutics, JUL 2, 2026, View Source [SID1234669056])