Market Intelligence, Clinical Progress, and High-Purity Reagents for Oncology and Metabolic Disease Development.
TarMart Solution Ecosystem & Related Targets
Comprehensive reagent toolkit for ACSL5 drug discovery. Select your modality below:
| Component / Network | Product Description | Product Link |
|---|---|---|
| Antigen | ACSL5 Full-Length Recombinant Protein HEK293 Expressed (Native Glycosylation), High purity (>95%), Endotoxin <1EU/ug. Sequence Verified. Theoretical MW validated. |
View ACSL5 Products |
| Gene Delivery | ACSL5 ORF Lentivirus Particles Full-length ORF for stable cell line construction. CMV promoter. Puromycin selection. |
View ACSL5 Products |
| Benchmark Ab | Anti-ACSL5 Recombinant Antibody Research-grade monoclonal positive control. Sequence Verified. |
View ACSL5 Products |
| Validator | ACSL5 siRNA Set (3 Unique Targets) For knockdown verification and specificity controls. Sequence Verified. |
View ACSL5 Products |
| Homolog Panel | ACSL4 Recombinant Protein Subfamily selectivity screening and ferroptosis regulator. Sequence Verified, >95% purity. |
View ACSL4 Products |
| Pathway Partner | CPT1A Recombinant Protein Mitochondrial fatty acid oxidation node. For combination therapy screening. |
View CPT1A Products |
| Lipogenesis Counterpart | FASN Recombinant Protein De novo lipogenesis pathway comparison. Sequence Verified. |
View FASN Products |
| Critical Assay Challenge | The TarMart Advantage (Technical Spec) |
|---|---|
| ACSL Subfamily Selectivity (ACSL1/3/4/6) | Homolog Panel available with strict sequence verification by mass spec. Human/Mouse/Cyno ortholog proteins >95% purity. |
| Enzymatic Activity Screening | Full-length ACSL5 with native membrane association preserved. Theoretical MW confirmed. Endotoxin controlled for cellular assays. |
| Cellular Validation | Validated siRNA included for specificity checks. Lentivirus particles for stable overexpression/knockdown cell line construction. |
| Drug Resistance Profiling | Catalytic site mutant variants available (rational design) for selectivity testing and resistance prediction. |
Live ACSL5 R&D Tracker
Market data changes daily. Access the latest global pipeline status directly:
Global Clinical Landscape & Future Outlook
The race for ACSL5-targeted therapeutics is intensifying at the intersection of metabolic disease and oncology. As a critical node in long-chain fatty acid activation, ACSL5 plays a key role in intestinal lipid absorption, diet-induced obesity, MASLD, and lipid-dependent cancers including colorectal, prostate, and hepatocellular carcinoma. The therapeutic paradigm is shifting from broad-spectrum modulators (which faced toxicity hurdles) toward isoform-selective ACSL5 inhibitors that can uncouple energy production from membrane biosynthesis in cancer cells while preserving physiological lipid homeostasis. Current development focuses on two distinct vectors: (1) small molecule inhibitors for metabolic diseases (NASH/NAFLD) targeting hepatic steatosis, and (2) oncology indications exploiting lipid addiction in aggressive tumor subtypes. The next wave of R&D is targeting combination regimens with checkpoint inhibitors and ferroptosis inducers, necessitating sophisticated selectivity profiling against the closely related ACSL4 isoform. As first-generation pan-ACSL inhibitors like Triacsin C demonstrated unacceptable cardiac and systemic toxicity, the key differentiator for next-generation molecules is absolute isozyme selectivity, particularly against ACSL1/3/4/6.
Key Mutations and Resistance Profiling
Several mutations in ACSL5 have been documented, providing critical insights for drug development and resistance monitoring. The common variant rs3736946 (dbSNP) represents a population-level polymorphism. A somatic mutation identified in colorectal cancer samples (UniProt VAR_036377) highlights the potential for acquired resistance during therapy. The DIAR13-associated mutation (UniProt VAR_088452) results in loss of oleoyl-CoA ligase activity without affecting subcellular localization, providing a valuable tool for distinguishing enzymatic vs. non-enzymatic functions. TarMart offers rationally designed catalytic site mutant variants for selectivity testing and resistance prediction, enabling early assessment of mutation-driven escape mechanisms.
Competitive Modality & Indication Snapshot
| Modality | Representative Players | Key Indications | Critical Assay Need (Why TarMart?) |
|---|---|---|---|
| Small Molecule Inhibitor | Early-stage biotechs, Academic consortia | NASH, NAFLD, Colorectal Cancer, Prostate Cancer | Enzymatic Activity Assay (Need full-length, membrane-associated protein with native conformation) |
| siRNA / ASO | Liver-targeted delivery platforms | Metabolic Syndrome, Hyperlipidemia, NAFLD | Knockdown Validation (Need validated siRNA and lentivirus for stable cell lines) |
| PROTAC / Degrader | Preclinical innovators | Refractory GI Tumors, Solid Tumors | Cell-based Degradation Assay (Need stable ORF cell lines for ubiquitination studies) |
| Combination Therapy | Oncology immunotherapy developers | Lipid-addicted solid tumors | Pathway Analysis (Need CPT1A/FASN parallel screening panels) |
| Allosteric Modulators | Academic drug discovery programs | Obesity, Type 2 Diabetes | Mutant Protein Panel (Need catalytic site variants for MOA confirmation) |