2. Signaling Pathways
  3. Cytoskeleton
  4. Arp2/3 Complex
  5. Arp2/3 Complex Inhibitor

Arp2/3 Complex Inhibitor

Arp2/3 Complex Inhibitors (11):

Cat. No. Product Name Effect Purity
  • HY-N6682
    Cytochalasin D
    		Inhibitor 99.79%
    Cytochalasin D (Zygosporin A) is a potent actin polymerization inhibitor, could be derived from fungus. Cytochalasin D has cell-permeable activity. Cytochalasin D inhibits the G-actin–cofilin interaction by binding to G-actin. Cytochalasin D also inhibits the binding of cofilin to F-actin and decreases the rate of both actin polymerization and depolymerization in living cells. Cytochalasin D can reduce exosome release, in turn reducing the amount of survivin present in the tumour environment. Cytochalasin D induces phosphorylation and cytoplasmic retention of Yap.
  • HY-16926
    CK-666
    		Inhibitor 99.17%
    CK-666 is a cell-permeable actin-related protein Arp2/3 complex inhibitor (IC50=12 μM). CK-666 binds to Arp2/3 complex, stabilizes the inactive state of the complex, blocking movement of the Arp2 and Arp3 subunits into the activated filament-like (short pitch) conformation.
  • HY-16931
    SMIFH2
    		Inhibitor 98.45%
    SMIFH2 is a formin specific inhibitor. SMIFH2 inhibits actin polymerization by Formins and affects the actin cytoskeleton.
  • HY-16929
    Latrunculin A
    		Inhibitor ≥98.0%
    Latrunculin A (LAT-A), found in the red sea sponge Latrunculia magnifica, is a G-actin polymerization inhibitor. Latrunculin A binds to actin monomers and inhibits polymerization of actin with Kds of 0.1, 0.4, 4.7 μM and 0.19 μM for ATP-actin, ADP-Pi-actin, ADP-actin and G-actin, respectively. Latrunculin A has effective anti-metastatic properties for cancer research. Latrunculin A blocks cell migration.
  • HY-114657A
    Benproperine phosphate
    		Inhibitor 99.35%
    Benproperine phosphate is an orally active, potent actin-related protein 2/3 complex subunit 2 (ARPC2) inhibitor. Benproperine phosphate attenuates the actin polymerization rate of action polymerization nucleation by impairing Arp2/3 function. Benproperine phosphate has the potential for a cough suppressant and suppresses cancer cell migration and tumor metastasis.
  • HY-15892
    CK-636
    		Inhibitor 99.92%
    CK-636 is a cell permeable inhibitor of Arp2/3 complex, that could inhibit actin polymerization, with IC50 values of 4 μM, 24 μM and 32 μM for human, fission yeast and bovine, respectively. CK636 blocks cell migration.
  • HY-16927
    CK-869
    		Inhibitor 99.74%
    CK-869 is an Actin-Related Protein 2/3 (ARP2/3) complex inhibitor, with an IC50 of 7 μM.
  • HY-12534
    Wiskostatin
    		Inhibitor 99.58%
    Wiskostatin is a potent and selective inhibitor of neuronal Wiskott-Aldrich syndrome protein (N-WASP)-mediated actin polymerization. Wiskostatin causes a rapid, profound, and irreversible decrease in cellular ATP levels.
  • HY-P1045
    187-1, N-WASP inhibitor
    		Inhibitor 99.86%
    187-1, N-WASP inhibitor, a 14-aa cyclic peptide, is an allosteric neural Wiskott-Aldrich syndrome protein (N-WASP) inhibitor. 187-1, N-WASP inhibitor potently inhibits actin assembly induced by phosphatidylinositol 4,5-bisphosphate (PIP2) with an IC50 of 2 μM. 187-1, N-WASP inhibitor prevents the activation of Arp2/3 complex by N-WASP by stabilizing the autoinhibited state of the protein.
  • HY-126989
    19-O-Acetylchaetoglobosin A
    		Inhibitor
    19-O-Acetylchaetoglobosin A, a cytochalasan alkaloid, is a fungal metabolite originally isolated from C. globosum that has actin polymerization inhibitory and cytotoxic activities. 19-O-Acetylchaetoglobosin A is cytotoxic to HeLa cervical cancer cells.
  • HY-P1045A
    187-1, N-WASP inhibitor TFA
    		Inhibitor
    187-1, N-WASP inhibitor TFA, a 14-aa cyclic peptide, is an allosteric neural Wiskott-Aldrich syndrome protein (N-WASP) inhibitor. 187-1, N-WASP inhibitor TFA potently inhibits actin assembly induced by phosphatidylinositol 4,5-bisphosphate (PIP2) with an IC50 of 2 μM. 187-1, N-WASP inhibitor TFA prevents the activation of Arp2/3 complex by N-WASP by stabilizing the autoinhibited state of the protein.