Instructing tumors to self-destruct.
IMV-M™ is a MUC16×DR5 bispecific antibody that super-clusters death receptors to kill tumor cells directly — payload-free, immune-sparing, and engineered to work where antibody–drug conjugates can't.
Less than a year from IND.
IMV-M™ has cleared the substantive de-risking milestones. The research cell bank is complete, the clinical plan is drafted, and the principal investigator is engaged — with first-in-human dosing less than a year out.
IMV-M™'s Phase 1 will be led by Dr. Daniel Von Hoff — the investigator behind the approvals of gemcitabine, nab-paclitaxel, and nanoliposomal irinotecan — at leading U.S. cancer centers. TGen's lab independently replicated IMV-M™'s anti-tumor efficacy in a foundation-funded study.
One molecule that turns a tumor antigen into a kill switch.
MUC16 (CA125) is abundant on the surface of several solid tumors and largely absent from healthy tissue. IMV-M™ uses it as a scaffold.
- 1Multiple IMV-M™ molecules bind a single MUC16 protein on the cancer-cell surface.
- 2That clustering forces the antibody's DR5 arms to super-cluster death receptors — only on MUC16-positive cells.
- 3DR5 super-clustering triggers the apoptosis pathway. The cell executes its own death — no payload, no immune activation.
Cytotoxic activity and safety characterization of IMV-M™, a MUC16 × DR5 bispecific antibody
- Shed CA125 does not neutralize IMV-M™ at clinically relevant concentrations — answering the central concern for MUC16-directed therapy.
- Anti-drug antibodies do not cause off-target liver toxicity — the failure mode that halted prior DR5 agonists.
- Multivalent engagement — not surface crowding — drives the killing, confirming the design.
Designed around the reasons targeted therapies fail.
Works where ADCs can't
Active in tumors with low-to-moderate MUC16 — the response pattern that predicts broad clinical efficacy in approved ADCs, not just the rare high-expressors.
No payload toxicity
The mechanism is a biological signal, not a delivered poison. Without MUC16-driven clustering, IMV-M™ does nothing — safety is built into the design.
A new patient population
Eligibility is non-overlapping with DXd-class ADCs, and free of their lung and hematologic platform toxicities.
Resistance-agnostic
Drug resistance doesn't confer resistance to apoptosis. Most tumors lack the machinery to suppress the death pathway IMV-M™ activates.
A lead asset, and a platform behind it.
IMV-M™ leads the way to the clinic. The Cancerlysin™ platform applies the same apoptosis engine to new tumor antigens.
Cancerlysin™ platform
A plug-and-play apoptosis engine: any tumor-selective antigen becomes a scaffold for tumor-restricted DR5 super-clustering. New targets open to partnering.
Three peer-reviewed papers.
The mechanism, efficacy, and safety of IMV-M™ and the Cancerlysin™ platform — in the literature.
Cytotoxic activity and safety characterization of IMV-M™, a MUC16 × DR5 bispecific antibody
Read →A bispecific anti-MUC16/anti-DR5 antibody achieves effective, tumor-selective DR5-mediated tumor regression
Read →Beyond ADCs: harnessing bispecific antibodies to directly induce apoptosis for targeted tumor eradication
Read →Open to partnering on new targets.
The Cancerlysin™ platform turns clinically validated tumor antigens into apoptosis-inducing therapeutics. We're seeking partners to expand it.