2. Signaling Pathways
  3. Metabolic Enzyme/Protease
  4. ACSL Family

ACSL Family

Long-chain acyl-CoA synthetase (ACSL) serves as a central regulatory node in cellular lipid metabolism, responsible for activating free long-chain fatty acids into acyl-CoAs, thereby channeling these fatty acids into downstream pathways such as oxidative energy production or complex lipid synthesis. The mammalian ACSL family comprises five isoforms-ACSL1, ACSL3, ACSL4, ACSL5, and ACSL6-which exhibit significant differences in their tissue distribution, subcellular localization, and substrate preferences[1].
Specifically, ACSL3 inhibits lipid peroxidation by enriching monounsaturated fatty acids, thereby protecting tumor cells from damage. ACSL4 is predominantly enriched in adrenal and brain tissues; it specifically favors the activation of 20-carbon polyunsaturated fatty acids (PUFAs), acts as a core executor driving ferroptosis, and participates in the JAK-STAT1-IRF1 signaling axis. In various malignancies-such as hepatocellular carcinoma and breast cancer-ACSL4 exerts pro-tumorigenic effects and is associated with poor prognosis. Conversely, ACSL5 is primarily distributed in the intestine, localizes to mitochondria, and prefers 16-18 carbon fatty acids; it suppresses the Wnt signaling pathway by mediating the palmitoylation of the Wnt2B protein, typically functioning as a tumor suppressor gene and exerting protective effects in pancreatic cancer. However, in gastric cancer, ACSL5 is aberrantly overexpressed due to promoter hypomethylation, which paradoxically promotes the proliferation and metastasis of tumor cells[1][2][3].
The expression of the ACSL family is under strict regulation by signaling pathways-such as JAK-STAT and PPAR-as well as epigenetic mechanisms; functional abnormalities within this family are closely implicated in various malignancies-including hepatocellular carcinoma and breast cancer-as well as metabolic disorders. Inhibitors specifically targeting ACSL4 and ACSL5-such as troglitazone and tolcapone-hold potential for clinical application in precisely disrupting tumor metabolism or mitigating tissue damage[1][2][3].

ACSL Family Isoform Specific Products:

ACSL Family Isoform Comparison
Cat. No. Product Name Effect Purity Chemical Structure
  • HY-RS00204
    ACSL6 Human Pre-designed siRNA Set A
    		Inhibitor

    ACSL6 Human Pre-designed siRNA Set A contains three designed siRNAs for ACSL6 gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control.
    ACSL6 Human Pre-designed siRNA Set A
  • HY-112005G
    DOPE (GMP)
    		Inhibitor
    DOPE GMP is DOPE (HY-112005) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. DOPE (Dioleoylphosphatidylethanolamine; 1,2-Dioleoyl-sn-glycero-3-phosphoethanolamine) is an orally active inhibitor of ferroptosis with anti-inflammatory and intestinal barrier maintenance activities. DOPE regulates the expression of ACSL4, SLC7A11 and GPX4 to restore the redox system balance, thereby reducing the levels of lipid peroxides, iron ions and intestinal inflammatory factors (IL-1β and IL-6). DOPE promotes the migration and proliferation of intestinal epithelial cells and increases the level of tight junction proteins; it also destabilizes endosomal membranes, mediates the conjugation of RVG peptides with mesenchymal stem cell-derived exosomes to enhance brain targeting. DOPE can be applied to research related to neonatal necrotizing enterocolitis and Alzheimer's disease.
    DOPE (GMP)
  • HY-174345
    Ferroptosis inducer-8
    		Activator
    Ferroptosis inducer-8 is a ferroptosis inducer with high selectivity for other cell death mechanism. Ferroptosis inducer-8 induces ferroptosis by affecting ACSL4, GPX4, and FTH1, thereby disrupting intracellular iron homeostasis and the GSH/GPX4 antioxidant defense system, ultimately leading to the accumulation of lipid peroxidation. Ferroptosis inducer-8 also induces ROS production. Ferroptosis inducer-8 inhibits tumor growth and can be used for research of triple-negative breast cancer (TNBC).
    Ferroptosis inducer-8
  • HY-183791A
    Ferroptosis/apoptosis inducer-5
    		Activator
    Ferroptosis/apoptosis inducer-5 (Compound 14) is an orally active inducer of Ferroptosis and Apoptosis. Ferroptosis/apoptosis inducer-5 downregulates GPX4, upregulates ACSL4, promotes ROS production, activates the Caspase cascade, induces Mitochondrial dysfunction, and alters the Bcl-2/Bax balance. Ferroptosis/apoptosis inducer-5 significantly inhibits tumor growth in a pancreatic cancer xenograft mouse model. Ferroptosis/apoptosis inducer-5 can be used for the research of pancreatic cancer.
    Ferroptosis/apoptosis inducer-5
  • HY-RS00203
    ACSL5 Human Pre-designed siRNA Set A
    		Inhibitor

    ACSL5 Human Pre-designed siRNA Set A contains three designed siRNAs for ACSL5 gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control.
    ACSL5 Human Pre-designed siRNA Set A
  • HY-155851
    Lepadin E
    		Activator
    Lepadin E is a significantly cytotoxic ferroptosis inducer that induces iron death through the classical p53-SLC7A11-GPX4 pathway. Lepadin E promoted p53 expression, decreases SLC7A11 and GPX4 levels, and leads to increased ROS and lipid peroxide production, and upregulated ACSL4 expression, thus causes cell death. Lepadin E has significant antitumor effect.
    Lepadin E
  • HY-155852
    Lepadin H
    		Activator
    Lepadin H is a ferroptosis inducer and apoptosis inducer with in vitro cytotoxicity and in vivo antitumor efficacy against cancer cells. Lepadin H reduces GPX4 and SLC7A11 levels, increases p53 and ACSL4 expression, drives lipid hydroperoxide production, elevates reactive oxygen species (ROS) levels, reduces cellular glutathione (GSH) levels, induces lipid peroxidation and G2/M phase cell cycle arrest, and suppresses clonogenic growth and migration of cancer cells.Lepadin H can be used for the research of melanoma.
    Lepadin H
  • HY-186084
    ACSL5-IN-4
    ACSL5-IN-4 (the 9th compound in Table 115) is an ACS5 inhibitor, with its IC50 value for hACS5 being less than 100 nM. ACSL5-IN-4 can be used for research in digestive and oncological diseases.
    ACSL5-IN-4
  • HY-179384
    PROTAC FSP1 degrader 1
    		Activator
    PROTAC FSP1 degrader 1 is a highly efficient and selective PROTAC degrader targeting FSP1. PROTAC FSP1 degrader 1 significantly induces the accumulation of intracellular lipid peroxides. PROTAC FSP1 degrader 1 exhibits synergistic induction of ferroptosis with GPX4 inhibitors. PROTAC FSP1 degrader 1 can induce ROS production. PROTAC FSP1 degrader 1 upregulates the mRNA expression of ferroptosis-related proteins (GPX4, FTH1, ACSL4, TfR1, FSP1). PROTAC FSP1 degrader 1 can be used for the study of triple-negative breast cancer.
    PROTAC FSP1 degrader 1
  • HY-121246R
    Fluorofenidone (Standard)
    		Activator
    Fluorofenidone (Standard) is the analytical standard of Fluorofenidone (AKF-PD) (HY-121246). This product is intended for research and analytical applications. Fluorofenidone is an orally active compound with anti-fibrotic, antioxidant, and anti-inflammatory pharmacological effects. Fluorofenidone downregulates the expression of ACSL4, upregulates GPX4 expression and inhibits the NF-κB signaling pathway to alleviate inflammation and fibrosis. Fluorofenidone ameliorates cholestasis and fibrosis by inhibiting hepatic Erk/-Egr-1 signaling and Tgfβ1/Smad pathway in mice. Fluorofenidone demonstrates protective effects against chronic lung injury in mice. Fluorofenidone can be used for the study of chronic obstructive pulmonary disease (COPD), pulmonary interstitial fibrosis (PIF) and non-small cell lung cancer (NSCLC).
    Fluorofenidone (Standard)
  • HY-121246S
    Fluorofenidone-d3
    		Inhibitor
    Fluorofenidone-d3 (AKF-PD-d3) is deuterium labeled Fluorofenidone (AKF-PD) (HY-121246). Fluorofenidone is an orally active compound with anti-fibrotic, antioxidant, and anti-inflammatory pharmacological effects. Fluorofenidone downregulates the expression of ACSL4, upregulates GPX4 expression and inhibits the NF-κB signaling pathway to alleviate inflammation and fibrosis. Fluorofenidone ameliorates cholestasis and fibrosis by inhibiting hepatic Erk/-Egr-1 signaling and Tgfβ1/Smad pathway in mice. Fluorofenidone demonstrates protective effects against chronic lung injury in mice. Fluorofenidone can be used for the study of chronic obstructive pulmonary disease (COPD), pulmonary interstitial fibrosis (PIF) and non-small cell lung cancer (NSCLC).
    Fluorofenidone-d<sub>3</sub>
  • HY-RS25472
    Acsl3 Rat Pre-designed siRNA Set A
    		Inhibitor

    Acsl3 Rat Pre-designed siRNA Set A contains three designed siRNAs for Acsl3 gene (Rat), as well as a negative control, a positive control, and a FAM-labeled negative control.
    Acsl3 Rat Pre-designed siRNA Set A
  • HY-RS18983
    Acsl3 Mouse Pre-designed siRNA Set A
    		Inhibitor

    Acsl3 Mouse Pre-designed siRNA Set A contains three designed siRNAs for Acsl3 gene (Mouse), as well as a negative control, a positive control, and a FAM-labeled negative control.
    Acsl3 Mouse Pre-designed siRNA Set A
  • HY-RS24003
    Acsl1 Rat Pre-designed siRNA Set A
    		Inhibitor

    Acsl1 Rat Pre-designed siRNA Set A contains three designed siRNAs for Acsl1 gene (Rat), as well as a negative control, a positive control, and a FAM-labeled negative control.
    Acsl1 Rat Pre-designed siRNA Set A
  • HY-RS26482
    Acsl5 Rat Pre-designed siRNA Set A
    		Inhibitor

    Acsl5 Rat Pre-designed siRNA Set A contains three designed siRNAs for Acsl5 gene (Rat), as well as a negative control, a positive control, and a FAM-labeled negative control.
    Acsl5 Rat Pre-designed siRNA Set A
  • HY-RS27364
    Acsl6 Rat Pre-designed siRNA Set A
    		Inhibitor

    Acsl6 Rat Pre-designed siRNA Set A contains three designed siRNAs for Acsl6 gene (Rat), as well as a negative control, a positive control, and a FAM-labeled negative control.
    Acsl6 Rat Pre-designed siRNA Set A
ACSL Family Isoform Comparison

Your Search Returned No Results.

Sorry. There is currently no product that acts on isoform together.

Please try each isoform separately.