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])

On March 5, 2026 Quanta Therapeutics, a privately held, clinical-stage biopharmaceutical company leading the development of innovative oral therapeutics for RAS-driven cancers, reported the presentation of data demonstrating its oral multi-KRAS inhibitors, G12D-preferring QTX3034 and G12V-preferring QTX3544, retain potent activity in the presence of known and novel mechanisms acquired from treatment with the pan-RAS(ON) tri-complex inhibitor, daraxonrasib. The presentation will be given at the AACR (Free AACR Whitepaper) Special Conference in Cancer Research: RAS Oncogenesis and Therapeutics being held March 5-8, 2026, in Los Angeles, California.

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"While pan-RAS tri-complex inhibitors have demonstrated a broad potential to treat various KRAS-driven cancers, acquired resistance mechanisms have limited the depth and durability of clinical benefit, particularly with heterogeneous tumors such as colorectal cancer," said Cameron Pitt, PhD, Co-Founder and Chief Operating Officer of Quanta Therapeutics. "Our data confirm previously reported resistance pathways, identify novel mutations uniquely associated with this class of therapies and demonstrate the ability of our drug candidates to overcome key tri-complex inhibitor resistance mechanisms."

Pitt added, "As the field continues to evolve, patients with KRAS-mutated cancers will require multiple distinct drug mechanisms to combat the propensity for RAS reactivation. Studies like this deepen our understanding of resistance biology and can inform strategies to optimize patient outcomes. Supported by encouraging clinical data to date, along with these new preclinical findings, we believe our approach to direct KRAS inhibition may provide a valuable therapeutic option for KRAS-mutant cancer patients with diverse treatment histories including a prior tri-complex inhibitor."

AACR-RAS presentation information:
Title: Resistance to the pan-RAS(ON) tri-complex inhibitor daraxonrasib is overcome by direct multi- KRAS inhibitors, QTX3034 and QTX3544.
Date and Time: Saturday, March 7, 2026; 11:45 am – 12:15 pm
Session Name: Poster Session B
Abstract Number: B033

(Press release, Quanta Therapeutics, MAR 5, 2026, View Source [SID1234663317])

On March 5, 2026 BridgeBio Oncology Therapeutics, Inc. ("BBOT") (Nasdaq: BBOT), a clinical-stage biopharmaceutical company focused on RAS-pathway malignancies, reported financial results for the fourth quarter and full year ended December 31, 2025, and provided a business update, including highlights of pipeline progress.

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BBOT’s portfolio of clinical-stage RAS-pathway inhibitors is designed to enable direct dual inhibition of KRAS in both its ON and OFF states, panKRAS coverage across major KRAS mutations, and disruption of RAS:PI3Kα activation. Together, these assets uniquely position BBOT to achieve safe, concurrent, high-level suppression of both the MAPK and PI3Kα pathways through a wholly owned internal combination strategy.

"2025 was a transformational year for BBOT as we debuted as a public company and advanced all three of our internally discovered RAS and PI3Kα programs into clinical development," said Eli Wallace, PhD, Chief Executive Officer of BBOT. "The preliminary safety and antitumor data across BBO-8520, BBO-11818, and BBO-10203 are consistent with a differentiated therapeutic index profile and reinforce the combination thesis underlying our portfolio. We believe we are uniquely positioned to pursue concurrent suppression of both the MAPK and PI3Kα pathways — a strategy made possible by our wholly owned, internally designed platform, which we do not believe exists elsewhere in the industry. With multiple data readouts expected in the second half of 2026 and cash runway into 2028, we remain focused on generating the data that demonstrate what this portfolio can do."

Key Clinical Highlights & Upcoming Milestones

BBO-8520: An orally bioavailable small molecule direct inhibitor targeting both the ON and OFF states of KRAS. BBO-8520 combined with pembrolizumab at active dose levels demonstrated antitumor activity with a potentially differentiated liver toxicity profile, a profile not previously observed with OFF inhibitors.

On January 9, 2025, BBOT announced the U.S. Food and Drug Administration ("FDA") granted Fast Track designation to BBO-8520 for the treatment of adult patients with previously treated, KRASG12C mutated metastatic non-small cell lung cancer (NSCLC).
On January 7, 2026, BBOT announced new clinical data from the ongoing Phase 1 ONKORAS-101 trial (NCT06343402).
As of November 15, 2025, BBO-8520 monotherapy in patients with KRASG12C NSCLC showed a 65% objective response rate (ORR) and a 68% 6-month progression-free survival (PFS), with 83% of patients eligible for 6-month follow-up remaining on treatment for ≥6 months, alongside a potentially differentiated safety profile.
Encouraging early efficacy signals were seen in patients with KRASG12C and STK11 and/or KEAP1 co-mutants, where all five initial patients achieved partial response (PR).
BBO-8520 in combination with pembrolizumab, at active dose levels, demonstrated promising efficacy data and a distinct safety profile, including a potentially differentiated liver toxicity profile.
Updated clinical data are expected in the second half of 2026 and internal combination with BBO-10203 is anticipated to open later in 2026.
BBO-11818: An orally bioavailable small molecule panKRAS inhibitor that targets mutant KRAS in both the ON and OFF states. BBO-11818 demonstrated a confirmed PR in a patient with pancreatic ductal adenocarcinoma (PDAC) — the first clinically confirmed monotherapy panKRAS response in pancreatic cancer — alongside additional tumor reductions at higher dose levels and no dose-limiting toxicities.

On April 1, 2025, BBOT announced that the first patient was dosed with BBO-11818 in the ongoing Phase 1 KONQUER-101 trial (NCT06917079) for advanced solid tumors.
On October 23, 2025, BBOT presented preclinical data at the 2025 AACR (Free AACR Whitepaper)-NCI-EORTC AACR-NCI-EORTC (Free AACR-NCI-EORTC Whitepaper) International Conference on Molecular Targets and Cancer Therapeutics (EORTC-NCI-AACR) (Free ASGCT Whitepaper) (Free EORTC-NCI-AACR Whitepaper). The preclinical data demonstrated the potential of BBO-11818 as a potent panKRAS inhibitor targeting mutant KRAS in both the ON and OFF states, with selectivity over HRAS and NRAS.
On January 7, 2026, BBOT announced preliminary clinical data. BBO-11818 demonstrated encouraging early anti-tumor activity across dose levels and tumor types, including a partial response (PR) in a patient with PDAC with a 56% tumor reduction. The response was unconfirmed at the time of data cutoff but was subsequently confirmed. BBO-11818 monotherapy appeared generally tolerable with no dose-limiting toxicities (DLTs).
Updated clinical data are expected in the second half of 2026. Combination with BBO-10203 is anticipated to open later in 2026.
BBO-10203: An orally bioavailable small molecule with a novel mechanism of action designed to block the physical interaction between RAS and PI3Kα, inhibiting RAS-driven PI3Kα-AKT signaling in tumors. BBO-10203 achieved full target engagement at pharmacologically active exposures with no observed hyperglycemia and no baseline HbA1c or glucose restrictions.

On June 12, 2025, BBOT announced the publication of preclinical data supporting the potential for BBO-10203 to provide therapeutic benefit across multiple tumor types. The publication, titled "BBO-10203 inhibits tumor growth without inducing hyperglycemia by blocking RAS-PI3Kα interaction" was published in the peer-reviewed journal Science.
On October 25, 2025, BBOT presented preclinical data at the 2025 AACR (Free AACR Whitepaper)-NCI-EORTC AACR-NCI-EORTC (Free AACR-NCI-EORTC Whitepaper) International Conference on Molecular Targets and Cancer Therapeutics (EORTC-NCI-AACR) (Free ASGCT Whitepaper) (Free EORTC-NCI-AACR Whitepaper). Preclinical data showed BBO-10203 blocked RAS-mediated activation of PI3Kα and strongly inhibited pAKT signaling in tumor cells without affecting glucose metabolism. Robust monotherapy activity, as well as combination activity with BBO-8520 and BBO-11818, was observed at well-tolerated dose levels in a panel of KRAS mutant models.
On December 10, 2025, BBOT announced late-breaking preclinical data at the San Antonio Breast Cancer Symposium (SABCS). Preclinical data demonstrated BBO-10203 blocked RAS-mediated activation of PI3Kα, strongly inhibited pAKT signaling in tumor cells without inducing hyperglycemia, and showed robust anti-tumor activity both as monotherapy and in combination with standard of care (SOC) therapies in mutant or wild-type PIK3CA breast cancer models.
On January 7, 2026, BBOT announced preliminary clinical data from the ongoing Phase 1 BREAKER-101 trial (NCT06625775).
BBO-10203 demonstrated a differentiated safety profile with no hyperglycemia in patients without restrictions on baseline HbA1c and glucose levels.
In addition, BBO-10203 achieved target systemic exposure and rapid full target engagement.
Clinical benefit was observed in patients with colorectal cancer (CRC) (>80% 3L+) and hormone receptor positive breast cancer (HR+ BC) who were previously heavily treated and tumor reductions were observed in some patients.
Updated clinical data are expected in the second half of 2026 and internal combinations, including with BBO-8520 and BBO-11818, are anticipated to open later in 2026.
Other Key Corporate Updates

On August 11, 2025, BBOT announced the closing of its previously announced business combination with Helix Acquisition Corp. II (formerly Nasdaq: HLXB) ("Helix"), a special purpose acquisition company ("SPAC") sponsored by affiliates of Cormorant Asset Management, LP. On August 12, 2025, BBOT began trading under the new ticker symbol "BBOT" on the Nasdaq Global Market.
Fourth Quarter 2025 Financial Results

Cash Position: As of December 31, 2025, BBOT had cash, cash equivalents and marketable securities totaling $425.5 million, which is expected to provide cash runway into 2028.
Research and development (R&D) expenses: R&D expenses were $38.1 million for the fourth quarter of 2025 compared to $19.5 million for the fourth quarter of 2024. The increase in expenses was primarily due to increases in clinical trial expenses and manufacturing expenses for BBO-8520, BBO-11818, and BBO-10203.
General and administrative (G&A) expenses: G&A expenses were $5.3 million for the fourth quarter of 2025 compared to $2.3 million for the fourth quarter of 2024. Changes in G&A expenses reflect the initiation of BBOT’s standalone operations and de-SPAC transaction.
Net Loss: Net loss was $38.8 million for the fourth quarter of 2025 compared to $19.7 million for the fourth quarter of 2024.
Full Year 2025 Financial Results

Research and development (R&D) expenses: R&D expenses were $121.2 million for the year ended December 31, 2025 compared to $73.1 million for the year ended December 31, 2024. The increase in expenses was primarily due to increases in clinical trial expenses and manufacturing expenses for BBO-8520, BBO-11818, and BBO-10203.
General and administrative (G&A) expenses: G&A expenses were $24.6 million for the year ended December 31, 2025 compared to $7.8 million for the year ended December 31, 2024. Changes in G&A expenses reflect the initiation of BBOT’s standalone operations and de-SPAC transaction.
Net Loss: Net loss was $134.0 million for the year ended 2025 compared to $74.3 million for the year ended 2024.

(Press release, BridgeBio Oncology Therapeutics, MAR 5, 2026, View Source [SID1234663316])