Registration Date 15 Nov 2022
Revision Date 15 Nov 2022



Medicine Pharmaceuticals

anticancer drug


Support for cancer therapies

Manufacturer's Description

OncoNano’s OMNI™ platform further highlights versatility of the core micelle technology to not only deliver therapeutic payloads but also directly activate a ubiquitous immune signaling molecule for cancer immunotherapy. OMNI is composed of proprietary polymers tailored to activate Stimulator of Interferon Genes (STING) which plays a crucial role in the generation of T cell immunity against solid tumors. OMNI polymers interact in a new and differentiating manner compared to small molecule STING agonists by not only binding to a complementary site on the STING protein but via polyvalent interactions: binding of multiple proteins to each polymer chain. Compared to small molecules that activate STING for 6-8 hours, OMNI’s polyvalent interactions result in condensation of OMNI-STING aggregates that stabilize STING activation for up to 48 hours which is important to induce infiltration of immune cells to turn the cold tumors into hot ones by immunotherapy.

OMNI polymers can encapsulate payloads such as STING agonists and tumor-specific antigens to produce drugs that are designed to be endocytosed where the low endosomal pH environment triggers micelle dissociation and release of both the payload and OMNI unimers within the cytosolic compartments of dendritic cells to illicit a T cell immune response. Our lead product candidate, ONM-501, is a preclinical phase novel immunotherapeutic for intratumoral administration comprised of OMNI encapsulated cGAMP, an endogenous small molecule STING agonist. The complementary combination of an initial burst STING activation by cGAMP and sustained STING activation by OMNI results in a robust STING activation profile that is not possible with either component alone. ONM-501 shows antitumor efficacy and when combined with checkpoint inhibitors such as anti-PD-1 produces a synergistic tumor killing effect in multiple cancer types. Preclinical data also shows evidence that ONM-501 activates CDN-resistant STING variants in 20% of patients and a low probability for off-target toxicities including cytokine storms.

The development of ONM-501 is supported by a grant from the Cancer Prevention and Research Institute of Texas (CPRIT).