BBOT debuted as a publicly traded company focused on optimized target coverage for patients with tumors driven by RAS and PI3Kα and a synergistic portfolio that is designed to enable targeted KRAS combinations

Advanced three ongoing Phase 1 clinical trials, with clinical data readouts from each program expected in 2026

Cash runway expected to fund BBOT operations into 2028

Appointed industry veteran Uneek Mehra as Chief Financial Officer

Continued clinical and operational progress of BBO-8520, an orally bioavailable small molecule direct inhibitor targeting both the ON and OFF states of KRAS. OFF-only inhibitors cannot covalently modify the ON-state; hence they need to maintain high concentration levels to capture free cycling KRAS G12C. ON/OFF inhibitors overcome this shortcoming. Dual ON/OFF inhibition allows BBO-8520 to fully capture the covalent mechanism of action, resulting in sustained pathway inhibition even after systemic drug levels decline, which we believe may enable a more potent and safer combination with pembrolizumab in patients with KRAS G12C mutant non-small cell lung cancer (“NSCLC”).

BBO-8520 has been shown to drive strong anti-tumor activity with favorable durability in multiple preclinical models. Early data from Phase 1 dose escalation showed a 60% confirmed overall response rate in KRAS G12C NSCLC patients.

The U.S. Food and Drug Administration (“FDA”) has granted Fast Track designation to BBO-8520 for the treatment of adult patients with previously treated, KRAS G12C-mutated metastatic NSCLC.

The ongoing Phase 1 ONKORAS-101 trial (NCT06343402) is evaluating BBO-8520 for patients with KRAS G12C mutant NSCLC. ONKORAS-101 is an open-label, multi-center Phase 1a/1b study designed to evaluate the safety, tolerability, preliminary antitumor activity, and pharmacokinetics of BBO-8520 as a single agent and in combination with pembrolizumab in patients with KRASG12C mutant NSCLC.

Updated clinical data are expected in the first quarter of 2026.

Continued clinical and operational progress of BBO-10203, an orally bioavailable small molecule with a novel mechanism of action designed to inhibit the physical interaction between RAS and PI3Kα, inhibiting RAS-driven PI3Kα-AKT signaling in tumors. BBO-10203 binds directly and covalently to the RAS-binding domain of PI3Kα, preventing its activation by KRAS, HRAS and NRAS, reducing downstream signaling and tumor growth. It is a protein-protein inhibitor and not a kinase inhibitor, enabling inhibition of RAS-driven PI3Kα-AKT signaling in tumors without the risk of hyperglycemia. Importantly, BBO-10203’s ability to block RAS activation of PI3Kα is agnostic to the mutational status of either RAS or PI3Kα. In addition to a potentially differentiated safety profile, BBO-10203 could be combined with direct KRAS inhibitors, such as BBO-8520 and BBO-11818, or drugs that target HER2 or ER receptors.

Preclinical data demonstrated that BBO-10203 blocks RAS-mediated activation of PI3Kα and strongly inhibits pAKT signaling in tumor cells without affecting glucose metabolism. In addition, robust monotherapy activity, as well as combination activity with KRAS inhibitors BBO-8520 and BBO-11818, as well as HER2 inhibitors and ER antagonists, were observed at well-tolerated dose levels. The combination of a KRAS inhibitor with a PI3Kα pathway inhibitor may maximize the response rate and reduce the development of adaptive resistance mechanisms due to full inhibition of both MAPK and PI3Kα signaling.

The ongoing Phase 1 BREAKER-101 trial (NCT06625775) is evaluating BBO-10203 for patients with locally advanced or metastatic HER2+ breast cancer, HR+/HER2- breast cancer, KRAS mutant colorectal cancer, and KRAS mutant non-small cell lung cancer.

Initial Phase 1 clinical data are expected in the first half of 2026.

Continued clinical and operational progress of BBO-11818, an orally bioavailable small molecule pan-KRAS inhibitor that targets mutant KRAS in both the ON and OFF states. Similar to BBO-8520, structure-based design was employed to target mutant KRAS in both the ON and the OFF states with strong affinity against KRAS G12D and KRAS G12V mutants. BBO-11818 has selectivity over HRAS and NRAS with the goal of achieving high levels of KRAS inhibition in human tumors. In addition, it has combination potential with BBO-10203 to mitigate the PI3Kα resistance pathway.

Preclinical data demonstrated suppression of MAPK signaling and viability in KRAS mutant cell lines, as well as anti-tumor activity across multiple KRAS G12D and KRAS G12V cell-derived xenograft (CDX) models. In addition, BBO-11818’s selectivity for KRAS was demonstrated by its >1000-fold lower potency against NRAS, HRAS, and BRAF-mutant cell lines. The preclinical activity of the combination of BBO-11818 with BBO-10203 was driven by a robust decrease in tumor cell proliferation and an increase in apoptosis; a combination benefit was also observed with cetuximab and anti-PD-1 treatment.

The ongoing Phase 1 KONQUER-101 (NCT06917079) trial is evaluating BBO-11818 for patients with locally advanced or metastatic KRAS mutant solid tumors.

Initial Phase 1 clinical data are expected in the second half of 2026.

In July, BBOT announced the appointment of Uneek Mehra as Chief Financial Officer. Mr. Mehra brings more than 28 years of global financial and business leadership experience across the biotechnology and pharmaceutical industries.

In August, 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. The business combination was approved by Helix’s shareholders on August 4, 2025, and closed on August 11, 2025. On August 12, 2025, BBOT began trading under the new ticker symbol “BBOT” on the Nasdaq Global Market.

Cash Position: As of September 30, 2025, BBOT had cash, cash equivalents and marketable securities totaling $468.3 million, which is expected to provide cash runway into 2028.

Research and development (R&D) expenses: R&D expenses were $35.1 million for the third quarter of 2025 compared to $17.9 million for the third quarter of 2024. The increase in expenses was primarily due to increases in clinical trial expenses and manufacturing expenses for BBO-8520, BBO-10203 and BBO-11818, and personnel-related expenses and stock-based compensation expenses related to additional headcount.

General and administrative (G&A) expenses: G&A expenses were $14.1 million for the third quarter of 2025 compared to $1.8 million for the third 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 $44.8 million for the third quarter of 2025 compared to $17.3 million for the third quarter of 2024.

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