BIK (BCL2 Interacting Killer) Drug Discovery Landscape & Assay Solutions

Navigating BH3-Only Protein Biology: High-Purity Recombinant BIK Antigens, Phospho-Mutants, and Lentiviral Systems for Apoptosis Pathway Drug Discovery.

TarMart Solution Ecosystem & Related Targets

Comprehensive reagent toolkit for BIK (NBK) drug discovery and BH3 profiling. Select your modality below:

Component / Network Product Description Product Link
Antigen (WT) BIK (BCL2L14) Full-Length Recombinant Protein
HEK293 Expressed, C-terminal His-tag, Endotoxin <1 EU/µg, Sequence Verified
View BIK Products
Antigen (Domain) BIK BH3 Domain Peptide (aa 51-78)
Synthetic / E. coli expressed, HPLC purity >95%, Theoretical MW verified
View BIK Products
Antigen (Mutants) BIK Phospho-Mutant Panel (T33A, T33D, S35A, S35D)
ERK-phosphorylation site variants for stability mechanism studies
View BIK Products
Gene Delivery BIK Promise-ORF Lentivirus (CMV promoter)
Full-length ORF for stable overexpression in cancer cell lines
View BIK Products
Validator BIK siRNA Set (3 unique targets)
For knockdown validation in apoptosis assays
View BIK Products
Reference Antibody Anti-BIK Rabbit Recombinant mAb (C-terminal)
High specificity for Western/IF validation
View BIK Products
Related Target: BCL2 Anti-apoptotic binding partner
Essential for BIK co-crystalization and competition assays
View BCL2 Products
Related Target: BCL2L1 (BCL-XL) Primary anti-apoptotic binding partner of BIK; essential for competitive binding assays and resistance bypass studies View BCL2L1 Products
Related Target: MCL1 Anti-apoptotic Bcl-2 family member; high-affinity target of BIK BH3 domain; critical resistance node View MCL1 Products
Related Target: BCL2L11 (BIM) Synergistic pro-apoptotic pathway; off-target screening control View BCL2L11 Products
Related Target: PMAIP1 (NOXA) Complementary BH3 profiling marker; selective BCL-2/MCL-1 binding View PMAIP1 Products

Critical Assay Challenges & The TarMart Advantage

Critical Assay Challenge The TarMart Advantage (Technical Spec)
Phospho-Regulation Stability Studies (ERK-mediated turnover) Phospho-site mutants (T33A/T33D, S35A/S35D) expressed in HEK293, Sequence Verified, High Purity (>95%)
BH3 Domain Folding Integrity (for BCL-2 binding) Helical domain antigens (aa 51-78) verified by Circular Dichroism (CD) compatibility; Endotoxin Controlled
Cross-Species Translation (Cyno/Mouse) Human/Mouse/Cyno BIK ortholog proteins available with >95% purity; Sequence alignment verified
Intracellular Target Validation Validated siRNA included for specificity checks; Lentivirus for stable expression in hard-to-transfect lines
Apoptosis Pathway Specificity BH3-only family panel (BIK, BIM, NOXA, BAD) for counter-screening; Theoretical MW match by Mass Spec
Quantifying binding kinetics against anti-apoptotic panel (BCL-2, BCL-XL, MCL-1) High-purity (>95%) recombinant BH3 domains and full-length proteins strictly verified by mass spectrometry and SDS-PAGE
Evaluating hyperactive mutant potency (BikDD: T33D/S35D) vs Wild-type Sequence-verified wild-type and phosphorylation-mimetic mutant proteins (T33D/S35D) available with rigorous quality checks
Preserving endoplasmic reticulum (ER) membrane localization in cellular assays Full-length ORF packaged in high-titer Lentivirus Premade Particles to guarantee native intracellular anchoring

Live BIK R&D Tracker

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

Global Clinical Landscape & Future Outlook

The BIK pro-apoptotic axis represents a critical but historically challenging frontier in apoptosis drug discovery. While direct therapeutic targeting of intracellular BH3-only proteins remains complex, BIK has emerged as a pivotal biomarker in BH3 profiling for predictive oncology and a mechanistic target in overcoming resistance to BCL-2 inhibitors. Unlike BAD, which is restricted to BCL-2 and BCL-XL, BIK exerts a broader pro-apoptotic pull by simultaneously neutralizing BCL-2, BCL-XL, and MCL-1 at the endoplasmic reticulum membrane.

The race for BIK-modulating therapeutics is intensifying, with major players shifting focus from traditional small-molecule BCL-2 inhibitors (Venetoclax analogs) toward proteolysis-targeting chimeras (PROTACs) and stapled peptide technologies that can engage intracellular BIK. Next-generation R&D is also exploring non-viral and viral gene delivery of hyperactive BIK mutants. Notably, the constitutively active BikDD mutant (T33D/S35D) driven by tumor-specific promoters has demonstrated potent anti-tumor efficacy in refractory breast, pancreatic, and lung cancer models. As lipid nanoparticle (LNP) and mRNA delivery platforms mature, transient intra-tumoral expression of engineered BIK variants represents a highly promising frontier for overcoming venetoclax and MCL-1 inhibitor resistance.

Competitive Modality & Indication Snapshot

Modality Representative Players Key Indications Critical Assay Need (Why TarMart?)
Stapled Peptides (BH3 Mimetics) Aileron Therapeutics, Genentech (Research) Solid Tumors, Lymphoma Helical BH3 Domain Antigens (Need high-purity, properly folded aa 51-78)
PROTACs (BIK Degraders) Arvinas, Nurix (BCL-2 family space) Refractory CLL, MM Phospho-Mutant Panels (T33/S35) for stability mechanism validation
Small Molecule (Stabilizers) AbbVie, AstraZeneca (Pipeline) Venetoclax-Resistant AML Full-Length BIK + BCL2 Co-incubation Assays (Need Human/Cyno orthologs)
Gene Therapy (Overexpression) Academic & Biotech Ventures (e.g., VISA-BikDD programs) Pancreatic Cancer, Triple-Negative Breast Cancer (TNBC) High-Titer Lentivirus (CMV/EF1a promoters) for stable cell line construction; Intracellular expression & apoptosis induction
BH3 Mimetic Combination AbbVie, Roche/Genentech CLL, AML, RCC Competitive binding assays (Need high-purity BIK + BCL-2 family panel)
Epigenetic Restoration Oncology Biotechs Gastric Cancer, Colorectal Cancer Expression validation (Need anti-BIK Benchmark Ab and siRNA)