The SNM Platform

Sunom Nucleoside Modification

A proprietary chemistry platform designed to re-engineer the nucleoside scaffold — extending a proven drug class into disease settings where resistance has limited its reach.

The Drug Class
Nucleoside analogs — gemcitabine, cytarabine, remdesivir, molnupiravir — have anchored modern oncology and antiviral medicine for decades. They remain among the most clinically validated, mechanistically understood, and commercially significant drug classes in medicine.
The Constraint
Their therapeutic reach is capped by well-characterized resistance pathways: enzymatic degradation in circulation, transporter-dependent cell entry, kinase-dependent activation, and DNA damage response. These mechanisms drive treatment failure across refractory cancers and limit development against emerging viral threats.
The SNM Approach
Rather than combining existing agents or reformulating legacy molecules, SNM modifies the nucleoside scaffold itself. The platform is designed to produce molecules that address multiple resistance mechanisms within a single compound — an engineering approach rather than a pharmacological workaround.

The result: a unified chemistry foundation capable of generating differentiated oncology and antiviral candidates — with novel IP and dual-use commercial potential.

Multi-Target

Designed to address multiple resistance mechanisms within a single molecule.

Proprietary

Novel IP covering SNM modifications.

Dual-Use

One chemistry foundation — oncology and antiviral applications.

Four Resistance Mechanisms. One Chemistry Platform.

Conventional nucleoside analogs encounter four well-characterized biological checkpoints. SNM chemistry is designed to bypass each one.

Preclinical Data Highlights

Head-to-head in vitro comparisons against Gemcitabine, the current standard of care, across multiple cancer cell lines.

0.3 µM

Sub-micromolar IC-50 Across 12+ Cell Lines

Pancreatic, NSCLC, Breast, CRC, Bladder

12+

Cancer Cell Lines Tested

Activity observed across solid tumor types

IC-90

Potency Advantage vs. Gemcitabine

Observed in most tested lines

Stable

Resistance to CDA Deamination

Retained in human serum stability assays

IC-90 Comparison: SNM Lead vs. Gemcitabine

Lower values indicate greater potency at near-complete cell kill.

SNM Lead Gemcitabine
Key Observation: SNM lead compounds achieve near-complete cell kill (IC-90) at concentrations where Gemcitabine produces only partial response — a clinically relevant difference given that meaningful outcomes in refractory disease depend on fractional kill well beyond the 50% threshold.

Why IC-90 Matters More Than IC-50

Most preclinical programs report IC-50 (50% growth inhibition). But clinical response in refractory cancers depends on near-complete tumor kill. IC-90 is a more translationally relevant potency metric — and the one where SNM chemistry consistently shows its greatest separation from Gemcitabine.

Why Not Just Reformulate Gemcitabine?

Prior efforts — nab-paclitaxel combinations, liposomal encapsulation, prodrug strategies — generally target a single resistance mechanism. SNM chemistry modifies the nucleoside scaffold itself, allowing a single molecule to be designed against multiple resistance pathways rather than engineered around one at a time.