Development Pipeline

An mRNA immunotherapeutic that clears HPV-16-driven high-grade cervical precancer (CIN2/3, cHSIL) without surgery. Given as four intradermal doses over six months, it is designed to drive lesion regression and HPV-16 clearance, replacing surgical excision.

HPV-16-positive high-grade squamous intraepithelial lesions (HSIL / CIN2/3), the direct precursor to cervical cancer (roughly a 9:1 precursor-to-cancer ratio). Natural expansion to CIN1, additional HPV strains, other HPV-driven cancers, and global low-resource settings.

Prior HPV immunotherapies reached proof-of-concept but missed the efficacy threshold for practice change. AI-optimized antigen design plus a potent LNP delivery engine target greater than 80% efficacy to replace LEEP. Non-excisional, it avoids LEEP's obstetric harms (cervical insufficiency, preterm birth) and up-to-25% recurrence and is simple and accessible.

No approved therapeutic exists. Near-term US HPV-16+ CIN2/3 is roughly $0.5-1B (LEEP runs ~250,000+ procedures/year); full HPV-16+ all-precancer exceeds $10B; the broader cervical-disease opportunity is framed at ~$8B. WHO’s priority is to treat precancers.

An AI-engineered mRNA vaccine that locks the Epstein-Barr virus surface glycoprotein in its most protective conformation. One vaccine with two wins: short-term prevention of EBV / mononucleosis and long-term prevention of the serious diseases EBV can trigger.

Infectious mononucleosis (~420,000 US doctor visits/year); multiple sclerosis (EBV associated with roughly 32x higher risk); EBV-linked cancers (lymphoma, gastric, nasopharyngeal); severe periodontitis; inflammatory disease. EBV infects ~95% of adults and persists for life.

The AI-designed prefusion-like antigen is validated across three herpesviruses (HSV-1, HSV-2, EBV), generating far more protective antibodies than conventional designs after decades without an approved EBV vaccine.

No approved EBV vaccine or immunotherapy. MS prevention and EBV-cancer prevention represent multibillion-dollar potential; recent EBV-vaccine M&A (a $1.55B acquisition by Lilly) signals appetite. Candidate for ARPA-H non-dilutive funding.

A prophylactic and therapeutic mRNA immunotherapy built on the same AI-engineered antigen platform to control HSV-1 and HSV-2 infection and achieve functional immune control.

Genital herpes, recurrent oral and genital herpes, neonatal herpes (herpes neonatorum), and herpes encephalitis. HSV-1/2 infect approximately 4 billion people (~70% global prevalence).

The AI-locked prefusion antigen raises far stronger neutralizing antibodies than conventional designs combined with a proprietary T-cell antigen against a target with decades of vaccine failure, spanning both prevention and functional-cure control.

Massive global unmet need with no cure or approved immunotherapy. Approximately $5M is needed to file the IND; positioned for Series A funding or partnering.

A partner-funded HBV therapeutic vaccine using Pinion's mRNA / LNP platform, aimed at functional cure of chronic hepatitis B.

Chronic hepatitis B.

A validated external partnership (Amoytop): partner-funded and heading to clinic, demonstrating the platform's out-licensing value.

Large chronic-HBV population; deal structure of ~$2M upfront plus milestones and royalties.

A DCAR (Dendritic Cell Antigen Reprogramming) mRNA immunotherapy that reprograms dendritic cells in vivo to drive potent, HLA-restricted CD8+ T-cell killing of neoantigen-expressing leukemic cells, eliminating minimal residual disease.

AML, which accounts for ~36% of US leukemias (~20,000 new cases and ~10,000 deaths per year; ~80% of adult cases are mutation-driven). Combination chemotherapy is poorly tolerated and bone-marrow transplant is curative only ~30% of the time.

DCAR overcomes the low CD8+ responses that limit conventional mRNA cancer vaccines and in vivo CAR-T. In HLA-A2.1 transgenic models roughly 50% of CD8+ T cells are neoantigen-specific, a wholly distinct mechanism of action. AML proof-of-concept de-risks the platform for solid tumors.

AML immunotherapy, with a candidate ARPA-H proposal (~$33M over three years) to establish clinical proof-of-concept.

A DCAR immunotherapy directed at shared KRAS-mutation neoantigens in solid tumors, extending the AML mechanism to high-prevalence cancers.

KRAS-mutant pancreatic ductal adenocarcinoma (PDAC, ~95% KRAS) and colorectal cancer (~45% KRAS). KRAS mutations are present in ~25% of all solid tumors.

The same DCAR mechanism drives strong, HLA-restricted CD8+ T-cell responses against shared KRAS neoantigens, leveraging AML proof-of-concept to de-risk a broad solid-tumor opportunity.

A KRAS-driven solid-tumor market exceeding $30B globally by 2030. Early-stage, currently G&A-funded discovery.