Market Intelligence, Clinical Progress, and High-Purity Reagents for Oncology Development.
TarMart Solution Ecosystem & Related Targets
Comprehensive reagent toolkit for PCNA drug discovery. Select your modality below:
| Component / Network | Product Description | Product Link |
|---|---|---|
| Antigen (WT Trimeric) | PCNA Native Trimeric Protein (HEK293 expressed) >95% purity, Endotoxin <1 EU/µg, sequence verified, MW ~87 kDa (trimer). | View PCNA Products |
| Antigen (Mutant) | PCNA K164R (Ubiquitination-defective) and ATLD2 (Hypomorphic UV repair mutant) proteins. Monomeric & trimeric forms available, mass spec verified. | View PCNA Products |
| Gene Delivery | PCNA Lentivirus / Promise-ORF (full-length ORF, CMV promoter) for stable cell line construction. | View PCNA Products |
| Benchmark Ab | Anti-PCNA Monoclonal Antibody (Clone PC10) – high affinity, IHC/Co-IP validated, recombinant positive control. | View PCNA Products |
| Validator | PCNA siRNA Set (3 unique sequences) for knockdown verification and specificity control. | View PCNA Products |
| Related Target A | FEN1 (Flap endonuclease 1) – key PIP-box interacting partner; synthetic lethality node. | View FEN1 Products |
| Related Target B | CDKN1A (p21) – cell cycle regulator that interacts via PIP-box; essential for PPI disruption assays. | View CDKN1A Products |
| Related Target C | POLH (DNA polymerase eta) – translesion synthesis polymerase, synergistic with PCNA. | View POLH Products |
| Related Target D | RFC1 (Replication Factor C subunit 1) – PCNA clamp loader; essential for clamp loading assays. | View RFC1 Products |
| Critical Assay Challenge | The TarMart Advantage (Technical Spec) |
|---|---|
| Targeting "Undruggable" Intracellular Protein | High-purity soluble PCNA proteins (WT & mutant) for rigorous SPR/BLI binding kinetic studies. |
| Trimerization & PIP-box Selectivity | WT and selected mutant proteins verified by SEC-HPLC & mass spec; >95% trimeric form ensures proper interface. |
| Cell Permeability & Nuclear Target Engagement | PCNA Lentivirus for stable U2OS/HeLa cell lines; compatible with CETSA and NanoBRET. |
| Ubiquitination & Post-Translational Modification Studies | K164R mutant (ubiquitination defective) and ATLD2 mutant available; sequence verified for mechanism validation. |
| Cross-species Preclinical Evaluation | Human/Mouse/Rat PCNA orthologs with >95% purity; conserved trimeric interfaces. |
| False Positives / Paralog Off-target (RFC / 9-1-1) | Ortholog counter-screen proteins (RFC complex, Rad9) available for selectivity assays. |
Live PCNA R&D Tracker
Market data changes daily. Access the latest global pipeline status directly:
Global Clinical Landscape & Future Outlook
The race for PCNA therapeutics is intensifying. Long considered an "undruggable" target due to its lack of deep active pockets and essential nature in all dividing cells, recent breakthroughs targeting the cancer-associated PCNA (caPCNA) isoform have shifted the paradigm. First-generation therapies such as AOH1996 (City of Hope) and T2-Amino-PCNA (Terpenoid Therapeutics) have reached clinical evaluation or advanced preclinical stages. The next wave of R&D focuses on allosteric small molecules, cell-penetrating peptides, and PROTACs that disrupt PCNA's protein-protein interactions (PPIs) via the PIP-box interface. Combination strategies with PARP inhibitors, platinum agents, and other DNA damage response (DDR) pathway modulators are being pursued to overcome resistance in BRCA-deficient and high-replication-pressure tumors. The field is rapidly moving from passive diagnostic marker (IHC proliferation index) to active therapeutic inhibition, requiring high-quality reagents tailored to trimeric PCNA and its mutant variants.
Competitive Modality & Indication Snapshot
| Modality | Representative Players | Key Indications | Critical Assay Need (Why TarMart?) |
|---|---|---|---|
| Small Molecule | City of Hope (AOH1996), Terpenoid Therapeutics | Solid Tumors, Drug-Resistant Cancers | Binding kinetics & PPI disruption (need high-purity WT/Mutant proteins for selectivity) |
| Peptide Inhibitor (PIP-box mimetic / Cell-Penetrating) | Various Biotechs (ATX-101), Academic Consortia | Colorectal, Ovarian, Refractory Cancers | Intracellular target engagement & PIP-box competition assay (need biotinylated PCNA + FEN1/RFC1 partners) |
| PROTAC / Degrader | Emerging Academic Programs & Startups | Broad Oncology, Refractory Neoplasms | Ternary complex formation & ubiquitination site validation (need K164R mutant and WT PCNA) |
| Synthetic Lethality Combo | Oncology Pharma Divisions | BRCA-deficient Tumors, High Replication Stress | Cell-based replication assay with stable PCNA knock-in/out lines (need Lentivirus) |
| Diagnostic / Research Ab | Various Commercial Suppliers | Pathology, DDR Research | IHC control & standardization (need high-spec recombinant antigen) |
Key Mutations and Variants in PCNA Research
PCNA mutations are rare in tumors but critical for understanding drug resistance and mechanism of action. Two key variants are routinely required in assay development:
- K164R: Blocks ubiquitination at K164, the major site for translesion synthesis (TLS) activation. Used to study resistance to PCNA-targeted therapies that rely on TLS bypass.
- ATLD2 (hypomorphic mutation affecting UV repair): A variant associated with ataxia-telangiectasia-like disorder 2 (ATLD2). This mutation impairs PCNA's role in DNA repair in response to UV damage, providing a tool to model synthetic lethality with ATR/ATM inhibitors.
TarMart offers both K164R and ATLD2 mutant proteins (monomeric and trimeric forms) to enable precise mechanism-of-action and selectivity studies.