A new way to kill cancer cells: instruct them to die.
Instead of delivering a poison, ImmuVia's Cancerlysin™ antibodies activate a tumor cell's own dormant suicide pathway — selectively, and only where the target antigen is present.
Beyond antibodies and ADCs.
Two generations of antibody therapy each solved one problem and left another. Cancerlysins™ address both.
Monoclonal antibodies
Most naked antibodies lack direct cytotoxic activity — with rare exceptions like Rituxan, Herceptin, and Avastin. Binding a cancer cell is rarely enough to destroy it.
Antibody–drug conjugates
Roughly fifteen approved out of hundreds evaluated. Inefficient internalization restricts ADCs to high-expressing antigens, and payload toxicity narrows the therapeutic window.
Cancerlysins™
A bispecific that initiates apoptosis through a biological pathway instead of a delivered poison — single-agent activity in pancreatic, lung, and ovarian tumors, without dose-limiting payload toxicity.
Super-clustering death receptors, on cue.
Prior DR5 agonists failed in the clinic because they could not drive enough receptor clustering to trigger apoptosis in vivo. IMV-M™ was engineered to solve exactly that — using a tumor-selective antigen as the scaffold for clustering.
- 1Multiple IMV-M™ molecules bind a single MUC16 (CA125) protein on the cancer-cell surface, using the antigen's repetitive structure as a scaffold.
- 2That clustering forces the antibody's DR5 arms to super-cluster Death Receptor 5 — but only on MUC16-positive cells.
- 3DR5 super-clustering activates the extrinsic apoptotic pathway. The cell executes its own death — no payload, no internalization, no immune activation.
The mechanism, tested and published.
- A sister MUC16×DR5 antibody binding MUC16 at a single epitope is non-cytotoxic where IMV-M™ kills — proving that multivalent engagement, not surface crowding, drives activity.
- Shed CA125 does not neutralize IMV-M™ at clinically relevant concentrations.
- Anti-drug antibodies do not cause off-target liver toxicity — the failure mode that halted prior DR5 agonists.
Single-agent activity, from a single injection.
In aggressive human xenograft models, one dose of IMV-M™ controls tumors that grow unchecked under vehicle and control antibodies.
Pancreatic adenocarcinoma
Lung adenocarcinoma
Active only where MUC16 is present.
Side-by-side xenografts make the selectivity visible: IMV-M™ eradicates MUC16-positive tumors and leaves MUC16-negative tumors to grow like vehicle.
MUC16-positive — on target
MUC16-negative — off target
Human tumor xenografts in immunodeficient mice; group means with error bars. Figures redrawn from ImmuVia's published and preclinical datasets.
Designed around the failure modes.
- Active in low-to-moderate antigen expressors. Response in tumors with modest target expression is the validated predictor of broad clinical efficacy for approved ADCs (Elahere™, Kadcyla®) — and where IMV-M™ is active, matching real patient tumors in ovarian, NSCLC, and pancreatic cancer.
- A non-overlapping patient population. Eligibility does not overlap with DXd-class ADCs, and the mechanism avoids their lung and hematologic platform toxicities.
- Resistance-agnostic. Drug resistance does not confer resistance to apoptosis; most tumors lack the machinery to suppress the death pathway IMV-M™ activates.
Safe because of how it works, not in spite of it.
With no cytotoxic payload, and no apoptosis unless MUC16 cross-links DR5, IMV-M™ does nothing in the absence of its target. The preclinical safety package bears this out.
The bivalent anti-DR5 antibody from which IMV-M™'s effector is derived (lexatumumab) was well tolerated at high doses in prior clinical testing.
Targeting tumors where outcomes remain poor.
See the path to the clinic.
IMV-M™ is at the IND-enabling stage, with first-in-human dosing less than a year out.