Investor and Partner Briefing
Kill cancer. Not immunity.
Onchilles Pharma is developing first-in-class therapeutic elastases that harness the ELANE pathway: broad, cancer-selective tumor killing that spares immune cells and turns every tumor destroyed into a source of systemic anti-tumor immunity.
The ELANE pathway in two minutes
Interested in the ELANE pathway, N17350, or partnership opportunities across the Onchilles pipeline? We would welcome the conversation.
Contact Us to Learn MoreCancer treatment has always meant compromise
Every established modality trades one thing for another. Breadth costs the immune system. Selectivity costs coverage. Immune activation fails the moment the tumor hides.
Toxic to cancer cells and equally toxic to the immune cells the body needs to fight disease.
Tumor heterogeneity means many cells lack the target. Those cells are missed, and they are the cells that grow back.
Checkpoint inhibitors release the brakes on immunity, but they fail when the tumor shields itself from immune recognition.
Onchilles is pursuing a new paradigm: broad tumor killing that is selective for cancer over healthy cells, delivered by a single agent that leaves the immune system intact to finish the job.
A vulnerability shared across solid tumors
Most solid tumors carry elevated levels of histone H1, a feature tied to their survival and fitness that drives genomic instability and aberrant gene expression. Normal cells do not. The ELANE pathway, discovered by Onchilles co-founder Lev Becker, PhD, turns that difference into a cancer-selective kill switch, independent of the tumor's genetic makeup or anatomical origin.
Selectivity comes from what cancer cells have in excess, not from a single mutation or surface target that a subset of cells can lack.
Because elevated histone H1 is a shared hallmark rather than a lineage marker, the same mechanism applies across tumor types.
Foundational ELANE pathway publication in Cell (2021), with a follow-on landmark study published in 2024.
From cell entry to immunogenic cell death
The cascade shown in the animation, step by step. Each step depends on the one before it, and the whole sequence depends on histone H1 being abundant.
- 01Entry
The therapeutic elastase enters the cancer cell.
- 02Cleavage
It cleaves the CD95 (FAS) receptor, releasing the C-terminal death domain into the cytoplasm.
- 03Complex formation
The liberated death domain binds histone H1, which cancer cells hold in excess.
- 04Disruption
The complex disrupts mitochondrial and DNA integrity, committing the cell to death.
- 05Immunogenic cell death
The dying cell releases tumor antigens and immunostimulatory signals (DAMPs) that recruit the immune system.
Healthy cells, including immune cells, keep histone H1 at low levels. They cannot form enough of the death domain–histone H1 complex to trigger the cascade, so at therapeutic doses they are largely unaffected.
Every destroyed tumor becomes its own vaccine
Conventional cytotoxics kill silently and take the immune system down with them. ELANE-mediated death is immunogenic: it kills the tumor in front of it and teaches the immune system to find the ones it cannot see.
One agent, two mechanisms: immediate, selective tumor destruction and systemic immune activation that can target distant disease.
Because immune cells survive the first wave, the antigens and danger signals released by dying cancer cells reach an intact immune system. Activated CD8+ T cells then recognize and attack tumors that were never treated directly.
- Trained by
- Tumor antigens plus immunostimulatory signals released during immunogenic cell death
- Effect
- Increased CD8+ T cell activity and reduction of untreated tumors in preclinical models
- Scope
- Observed in immunologically hot and cold tumors
- Durability
- Durable immune memory; improved activity of checkpoint inhibitors
Consistent across models, tumor types, and prior treatment
The mechanism has been validated across 11 cancer types, more than 80 genetically diverse cell lines, 41 patient samples, and over 25 animal models.
Robust efficacy in 11 cancer types
Including ovarian, breast, and colon cancer models.
Systemic anti-tumor immunity in hot and cold tumors
Robust immune activation regardless of baseline immune infiltration.
No observed resistance
No resistance mechanism has emerged upon repeat dosing.
Active where other therapies have failed
Efficacy retained in chemotherapy-resistant and checkpoint inhibitor-resistant tumors, with improved checkpoint inhibitor activity in combination.
Durable immune memory
Protection persists beyond the treated tumor in preclinical models.
Two routes into the same pathway
A tumor-directed lead already in the clinic, and a systemic follow-on designed to bring the mechanism to disease that cannot be injected.
N17350 (NEU-001)
Advanced solid tumors, including head and neck, skin, lung, and breast cancers; adults with chemotherapy-resistant or checkpoint inhibitor-refractory disease
NEU-002
Solid tumors
A first-in-human study of intratumoral N17350 evaluating safety, tolerability, and early signs of activity in adults with advanced solid tumors. Physicians can refer patients through ClinicalTrials.gov ID NCT07339176.
- 01IND clearance for N17350 (U.S. FDA)
- 02First patient dosed in OP-NEU-101
- 03NEU-002 preclinical data presented, AACR Annual Meeting 2026
- 04Trial-in-progress poster, ASCO Annual Meeting 2026
- 05Trial-in-progress presentation, ESMO Congress 2026 (upcoming)
One mechanism. Two effects. No compromise.
Selective tumor killing and systemic anti-tumor immunity from a single agent, now in the clinic. If the ELANE pathway belongs in your portfolio, let's talk.