Target-selective. Tumor-agnostic. Conditionally active.
EvoG — evolution-guided IgG — is a platform of engineered antibodies designed to remain inert in circulation and activate only at the surface of transformed cells.
Two operating companies apply the platform to distinct patient populations: Paratope Bio in pediatric solid tumors, Parallel Immunotherapeutics in adult oncology.
02 The Problem
Drug development in oncology is rate-limited by four problems that compound:
selectivity, escape, off-tumor toxicity, and time to clinical signal.
Most targeted therapies depend on a single antigen, a single mutation, or a high-burden neoepitope landscape. The result is a narrow patient population, a clear escape route through antigen loss, and a development path constrained to the indications where the target happens to be expressed at sufficient density.
Conditional approaches — masks, prodrugs, proximity inducers — engineer inertness around an active molecule. The active molecule still exists; the safety story rests on whether the gating element holds. Off-tumor toxicity remains a recurring late-stage failure mode.
Speed to clinical signal is the fourth constraint. Mechanisms that produce slow, indirect pharmacodynamic readouts extend dose escalation, delay go/no-go decisions, and absorb capital before signal.
THE PLATFORM
EvoG is built around a different starting point: antibody specificities that recognize transformation-associated molecular patterns — conserved surface features arising at malignant transformation, shared across tumor types, and largely absent on normal adult tissue.
Native inertness is preserved by design. The molecule activates only when clustering occurs at the density characteristic of transformed cells — analogous to adaptive antibodies prior to antigen exposure. Activity is local. Circulation is silent.
Pattern recognition substitutes avidity for ultra-high affinity to a single epitope. The mechanism does not depend on a single antigen or driver mutation, and it is not vulnerable to escape through antigen loss in the way single-target approaches are.
The platform is modality-flexible. Intrinsic killing, Fc-engineered effector function, and ADC formats are all accessible from the same scaffold.
WHY PEDIATRIC ONCOLOGY IS A DIFFERENT DISEASE
Childhood solid tumors carry roughly an order of magnitude fewer somatic mutations than adult carcinomas. Fewer neoantigens. Fewer driver mutations to inhibit. Fewer shared targets across patients. Checkpoint inhibitors have largely failed in pediatric solid tumors for this reason. Children receive adult-derived chemotherapy dosed down by body weight and pay the price in cardiotoxicity, secondary malignancies, growth arrest, and cognitive effects they carry for life.
A platform that recognizes transformation rather than mutation should produce its clearest signal precisely where mutation-directed therapies are weakest. Paratope Bio is built on that thesis.
TWO POPULATIONS, ONE PLATFORM
Paratope Bio — pediatric solid tumors. Development is supported by the National Pediatric Cancer Foundation and the Sunshine Project through the PIVOT preclinical-to-Phase 1 consortium.
Parallel Immunotherapeutics — adult oncology. The same platform applied to populations beyond the mutation-responsive subset, with implications for continuous surveillance and recurrence prevention.
Both companies sit under Sullivan & Company Holdings, a repository for the IP.
Further technical detail is shared under separate agreement.