Santolecan Pharmaceuticals is pleased to announce that its novel therapeutic candidate, CQ-0736, has been selected for an oral presentation at the prestigious AACR Annual Meeting 2026. The presentation will take place on April 21, 2026, from 2:35 PM to 2:50 PM in the session MS.CH01.01 – Targeted Therapies.

Titled “CQ-0736, a new polysaccharide-based therapeutic modality, targets pan-KRAS tumors with robust antitumor activity via macropinocytosis”, the presentation highlights a breakthrough approach to addressing one of the most challenging targets in oncology: RAS-driven cancers.

Oncogenic RAS mutations are present in approximately 20% of human cancers and remain among the most difficult to treat. These mutations not only drive uncontrolled tumor proliferation but also reprogram tumor metabolism, significantly enhancing macropinocytosis—a nutrient scavenging pathway that is largely inactive in normal tissues. Santolecan’s CQ-0736 is designed to exploit this unique biological vulnerability.

CQ-0736 is a first-in-class “Trojan horse” polysaccharide-based dual-drug conjugate. Built on a 100 kDa modified dextran backbone, it co-delivers docetaxel (DTX) and gamma-linolenic acid (GLA) directly into tumor cells via macropinocytosis. This innovative design transforms the tumor cell membrane from a passive barrier into an active transport interface, enabling highly selective and efficient intracellular drug accumulation.

Preclinical studies demonstrate the transformative potential of CQ-0736. In vitro, the compound showed significantly enhanced cytotoxicity compared to docetaxel alone across multiple pan-KRAS cancer cell lines, including KRASG12D, KRASG12C, and KRAS wild-type models. In vivo CDX and PDX xenograft studies further revealed greater than 95% tumor growth inhibition without observable toxicity or weight loss.

Importantly, in direct head-to-head comparisons, CQ-0736 outperformed both the investigational pan-RAS inhibitor RMC-6236 and the approved KRAS-targeted therapy Krazati (adagrasib). CQ-0736 demonstrated superior efficacy, longer-lasting responses, and reduced emergence of drug resistance.

Mechanistic studies confirmed that CQ-0736 exerts a dual antitumor effect—potently inhibiting cell proliferation (via reduction of PCNA and Ki-67) while inducing apoptosis (as evidenced by increased cleaved PARP). These findings highlight its ability to overcome key limitations associated with conventional chemotherapy and next-generation targeted therapies, including systemic toxicity and acquired resistance.

“CQ-0736 represents a paradigm shift in how we approach RAS-driven cancers,” said a company spokesperson. “By leveraging macropinocytosis as a tumor-selective delivery mechanism, we are turning a fundamental metabolic adaptation of cancer cells into a powerful therapeutic advantage.”

With its novel mechanism and compelling preclinical profile, CQ-0736 has the potential to redefine treatment strategies for patients with aggressive and treatment-resistant RAS-driven malignancies. Santolecan Pharmaceuticals looks forward to advancing this promising candidate toward clinical development and delivering meaningful impact to patients worldwide.