TP53 Y220C Drug Discovery Landscape & Assay Solutions

Market Intelligence, Clinical Progress, and High-Purity Reagents for TP53 Y220C Mutant Solid Tumor Therapeutics Development.

The Y220C mutation in TP53 creates a unique druggable crevice on the surface of the mutant protein, enabling small-molecule stabilizers to restore wild-type function. Leading the field is PMV Pharma's PC14586 (phase II), with others like Boehringer Ingelheim, Bayer, and Cullinan Oncology advancing candidates. The next wave targets combination strategies with MDM2/MDM4 inhibitors and immune checkpoint blockers.

TarMart Solution Ecosystem & Related Targets

Comprehensive reagent toolkit for TP53 Y220C drug discovery. Select your modality below:

Component / Network Product Description Product Link
Mutant Antigen TP53 Y220C Mutant Recombinant Protein (DBD / Full-Length). High purity (>95%), Endotoxin <1 EU/µg. Sequence Verified. Mutation confirmed by Mass Spec. View TP53 Y220C Products
WT Control TP53 Wild-Type DBD Protein. For selectivity screening and off-target liability assessment. View TP53 Products
Gene Delivery TP53 Y220C Promise-ORF / Lentivirus. Full-length ORF for stable cell line generation. View TP53 Y220C Products
Benchmark Ab Anti-TP53 (Clone DO-1) Recombinant Antibody. Pan detection for Western/IP. Also available: Y220C-specific antibody for mutation detection. View TP53 Y220C Products
Validator TP53 siRNA Set. For knockdown verification and rescue assays. View TP53 Products
Related Target A MDM2. E3 ubiquitin ligase & p53 negative regulator; major synergy combination target. View MDM2 Products
Related Target B MDM4. Synergistic negative regulator often overexpressed in tumors. View MDM4 Products
Related Target C CDKN1A (p21). Downstream effector & pharmacodynamic marker. View CDKN1A Products
Critical Assay Challenge The TarMart Advantage (Technical Spec)
Conformational Instability & Thermal Shift Screening High-purity monomeric Y220C protein (SEC verified, >95%) optimized for DSF/TSA. Endotoxin controlled for cell-based assays.
Mutant vs WT Selectivity Matched WT and Y220C pair with >95% purity; theoretical MW verified by Mass Spec. Ideal for SPR counter-screening.
Lack of Controls / False Positives Validated siRNA and clinical benchmark antibodies included for target-specificity and detection precision.
Structural Biology (Co-crystallization) Monomeric purity >95% by SEC-HPLC, suitable for co-crystal structure determination.

Live TP53 Y220C R&D Tracker

Market data changes daily. Access the latest global pipeline status directly:

Global Clinical Landscape & Future Outlook

The race for TP53 Y220C therapeutics is intensifying, with major players shifting focus from broad p53 modulators to precision small molecule stabilizers. PC14586 (PMV Pharma) is the first-in-class mutant-selective reactivator, now in phase II for advanced solid tumors (ovarian, breast, gastric). The next wave of R&D targets resistance mutations (e.g., Y220C double mutants) and rational combinations with MDM2/MDM4 pathway inhibitors, as well as immune checkpoint blockade. PROTAC degraders are in early research phase for refractory cancers. Indicative pipeline includes Bayer, Boehringer Ingelheim, and several early-stage biotechs.

Competitive Modality & Indication Snapshot

Modality Representative Players Key Indications Critical Assay Need (Why TarMart?)
Small Molecule Stabilizer PMV Pharma, Boehringer Ingelheim, Bayer Advanced Solid Tumors (Ovarian, Breast, Gastric, NSCLC, CRC) Thermal Shift Assay (need high-purity monomeric Y220C protein)
PROTAC / Degrader Early-stage Biotech Refractory Cancers (Solid & Hematologic) Degradation Assays (need mutant cell lines via lentivirus)
Combination Therapy (MDM2/PD-1) Various (with MDM2/MDM4 inhibitors) Refractory Solid Tumors Pathway Analysis (need pathway-related proteins: MDM2, MDM4, p21)

Key Scientific Context from Fact Payload

The Y220C mutation is a somatic hotspot in sporadic cancers. It abolishes phosphorylation at a key site, reduces interaction with ZNF385A, and is listed in dbSNP as rs587782646. These features underscore the importance of selective stabilization to restore p53 function without affecting wild-type.