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inhibitor ck 666  (MedChemExpress)


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    MedChemExpress inhibitor ck 666
    Pharmacological validation and inferred model of US3-mediated actin remodeling. ( a ) Schematic of the machine-learning workflow used to prioritize candidate F-actin regulators. Label-independent quantitative mass-spectrometry features were used for model training, whereas curated actin-regulator annotations were used only to define class labels. Prioritized candidates were subsequently selected for biological interpretation and experimental validation. ( b ) Flow-cytometric quantification of F-actin levels in N2A cells infected with WT HSV-1 or ΔUS3 HSV-1 and treated with the formin inhibitor SMIFH2, the Arp2/3 inhibitor <t>CK-666,</t> or both inhibitors. F-actin abundance was measured as the GeoMean MFI of Alexa Fluor 647–phalloidin at 0 and 24 hpi. Inhibition of either pathway partially attenuated the WT-associated reduction in F-actin, whereas combined inhibition prevented a statistically detectable reduction under the tested conditions. Data represent the mean ± SEM from three independent biological experiments. Statistical significance was assessed using two-way ANOVA followed by Šidák’s multiple-comparisons test. ns, not significant; * p < 0.05; **** p < 0.0001. ( c ) Proposed model integrating the US3 IP-MS interactome, machine-learning-prioritized proteins, and experimentally observed F-actin dynamics. Proteins detected in the US3 IP-MS interactome are distinguished from computationally prioritized or inferred proteins. Arrows represent proposed regulatory relationships, many of which may be indirect. The association between US3 and β-catenin was independently validated by reciprocal co-immunoprecipitation . During early infection, US3 is proposed to promote actin-polymerization programs involving Arp2/3- and formin-associated pathways, potentially supporting intracellular transport. At later stages, US3 is proposed to modulate Rho-family GTPase and cofilin signaling, contributing to stress-fiber disassembly and cytoskeletal remodeling associated with viral egress and spread. Myosin-associated motor complexes may contribute to cytoskeletal organization during both phases.
    Inhibitor Ck 666, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 35 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ck+666/CK-666/pmc13431605-51-16-18
    Average 95 stars, based on 35 article reviews
    inhibitor ck 666 - by Bioz Stars, 2026-09
    95/100 stars

    Images

    1) Product Images from "HSV-1 US3 Hijacks Conserved Actin Regulatory Complexes to Drive F-Actin Remodeling"

    Article Title: HSV-1 US3 Hijacks Conserved Actin Regulatory Complexes to Drive F-Actin Remodeling

    Journal: Viruses

    doi: 10.3390/v18070793

    Pharmacological validation and inferred model of US3-mediated actin remodeling. ( a ) Schematic of the machine-learning workflow used to prioritize candidate F-actin regulators. Label-independent quantitative mass-spectrometry features were used for model training, whereas curated actin-regulator annotations were used only to define class labels. Prioritized candidates were subsequently selected for biological interpretation and experimental validation. ( b ) Flow-cytometric quantification of F-actin levels in N2A cells infected with WT HSV-1 or ΔUS3 HSV-1 and treated with the formin inhibitor SMIFH2, the Arp2/3 inhibitor CK-666, or both inhibitors. F-actin abundance was measured as the GeoMean MFI of Alexa Fluor 647–phalloidin at 0 and 24 hpi. Inhibition of either pathway partially attenuated the WT-associated reduction in F-actin, whereas combined inhibition prevented a statistically detectable reduction under the tested conditions. Data represent the mean ± SEM from three independent biological experiments. Statistical significance was assessed using two-way ANOVA followed by Šidák’s multiple-comparisons test. ns, not significant; * p < 0.05; **** p < 0.0001. ( c ) Proposed model integrating the US3 IP-MS interactome, machine-learning-prioritized proteins, and experimentally observed F-actin dynamics. Proteins detected in the US3 IP-MS interactome are distinguished from computationally prioritized or inferred proteins. Arrows represent proposed regulatory relationships, many of which may be indirect. The association between US3 and β-catenin was independently validated by reciprocal co-immunoprecipitation . During early infection, US3 is proposed to promote actin-polymerization programs involving Arp2/3- and formin-associated pathways, potentially supporting intracellular transport. At later stages, US3 is proposed to modulate Rho-family GTPase and cofilin signaling, contributing to stress-fiber disassembly and cytoskeletal remodeling associated with viral egress and spread. Myosin-associated motor complexes may contribute to cytoskeletal organization during both phases.
    Figure Legend Snippet: Pharmacological validation and inferred model of US3-mediated actin remodeling. ( a ) Schematic of the machine-learning workflow used to prioritize candidate F-actin regulators. Label-independent quantitative mass-spectrometry features were used for model training, whereas curated actin-regulator annotations were used only to define class labels. Prioritized candidates were subsequently selected for biological interpretation and experimental validation. ( b ) Flow-cytometric quantification of F-actin levels in N2A cells infected with WT HSV-1 or ΔUS3 HSV-1 and treated with the formin inhibitor SMIFH2, the Arp2/3 inhibitor CK-666, or both inhibitors. F-actin abundance was measured as the GeoMean MFI of Alexa Fluor 647–phalloidin at 0 and 24 hpi. Inhibition of either pathway partially attenuated the WT-associated reduction in F-actin, whereas combined inhibition prevented a statistically detectable reduction under the tested conditions. Data represent the mean ± SEM from three independent biological experiments. Statistical significance was assessed using two-way ANOVA followed by Šidák’s multiple-comparisons test. ns, not significant; * p < 0.05; **** p < 0.0001. ( c ) Proposed model integrating the US3 IP-MS interactome, machine-learning-prioritized proteins, and experimentally observed F-actin dynamics. Proteins detected in the US3 IP-MS interactome are distinguished from computationally prioritized or inferred proteins. Arrows represent proposed regulatory relationships, many of which may be indirect. The association between US3 and β-catenin was independently validated by reciprocal co-immunoprecipitation . During early infection, US3 is proposed to promote actin-polymerization programs involving Arp2/3- and formin-associated pathways, potentially supporting intracellular transport. At later stages, US3 is proposed to modulate Rho-family GTPase and cofilin signaling, contributing to stress-fiber disassembly and cytoskeletal remodeling associated with viral egress and spread. Myosin-associated motor complexes may contribute to cytoskeletal organization during both phases.

    Techniques Used: Biomarker Discovery, Mass Spectrometry, Infection, Inhibition, Protein-Protein interactions, Immunoprecipitation

    Related Articles

    other:

    Article Title: ERM Inhibition Confers Ferroptosis Resistance through ROS‐Induced NRF2 Signaling
    Article Snippet: CK‐666 , MCE , Cat #HY‐16926.

    Inhibition:

    Article Title: UBC9-mediated SUMOylation of CORO1C drives lung adenocarcinoma progression via Arp2/3-dependent cytoskeletal remodeling
    Article Snippet: .. For pharmacological inhibition of the Arp2/3 complex, cells were treated with CK-666 (MCE, #HY-16926) at a final concentration of 100 μM. ..

    Article Title: UBC9-mediated SUMOylation of CORO1C drives lung adenocarcinoma progression via Arp2/3-dependent cytoskeletal remodeling.
    Article Snippet: .. For pharmacological inhibition of the AR TI CL E IN P RE SS Arp2/3 complex, cells were treated with CK-666 (MCE, #HY-16926) at a final concentration of 100 μM. ..

    Concentration Assay:

    Article Title: UBC9-mediated SUMOylation of CORO1C drives lung adenocarcinoma progression via Arp2/3-dependent cytoskeletal remodeling
    Article Snippet: .. For pharmacological inhibition of the Arp2/3 complex, cells were treated with CK-666 (MCE, #HY-16926) at a final concentration of 100 μM. ..

    Article Title: UBC9-mediated SUMOylation of CORO1C drives lung adenocarcinoma progression via Arp2/3-dependent cytoskeletal remodeling.
    Article Snippet: .. For pharmacological inhibition of the AR TI CL E IN P RE SS Arp2/3 complex, cells were treated with CK-666 (MCE, #HY-16926) at a final concentration of 100 μM. ..

    Article Title: G-CSF/NAMPT signaling drives neutrophil dysfunction and enhances bacterial infection susceptibility in cancer patients
    Article Snippet: .. CK‐666 (MedChemExpress), an Arp2/3 complex inhibitor, was dissolved in DMSO and added to the suspensions at a final concentration of 100 μM to inhibit actin branching, based on established in vitro protocols. ..

    Article Title: G-CSF/NAMPT signaling drives neutrophil dysfunction and enhances bacterial infection susceptibility in cancer patients.
    Article Snippet: .. CK‐666 (MedChemExpress), an Arp2/3 complex inhibitor, was dissolved in DMSO and added to the suspensions at a final concentration of 100 μM to inhibit actin branching, based on established in vitro protocols. ..

    Sonication:

    Article Title: ERM Inhibition Confers Ferroptosis Resistance through ROS‐Induced NRF2 Signaling
    Article Snippet: .. NSC305787 (MCE, #HY‐18931A) (dissolved in DMSO, sonicated for 5 min to make a 10 m m stock solution, aliquoted and stored at −80°C, re‐sonicated for 2 min before use); NSC668394 (MCE, #HY‐115492); Erastin (Sellcek, #S7242) (dissolved in DMSO to make a 10 m m stock solution, aliquoted and stored at −80°C, avoid repeated freeze‐thaw cycles); Jasplakinolide (SANTN CRUZ, #102396‐24‐7); ML385 (TargetMol, #T4360); Zinc Protoporphyrin IX (ZnPP, MCE, #HY‐101193); (1S, 3R)‐RSL3 (Selleck, #S8155); ML210 (MCE, #HY‐100003); Cytochalasin D (CytoD, Glpbio, #GC13440); tert‐butyl hydroperoxide (tBOOH, MACKLIN, #B802372‐50 mL); 2,3‐dimethoxy‐1,4‐naphthalenedione (DMNQ, MCE, #HY‐121026); MG‐132 (MCE, #HY‐13259); Z‐VAD (MCE, #HY‐16658B); CuCl 2 (Macklin, #C804816); Elesclomol (Macklin, #E864529); Ammonium tetrathiomolybdate (TTM, Macklin, #A828261); SB‐663825 (MCE, HY‐108333); SLK/STK10‐IN‐1 (MCE, #HY‐132868); Chloroquine (CQ, MCE, #HY‐17589A); CK‐666 (MCE, #HY‐16926); Ferrostatin‐1 (Fer‐1, MCE, #HY‐100579); Latrunculin A (LatA, Abcam, #ab144290); Brusatol (MCE, #HY‐19543); Liproxstatin‐1 (Lip‐1, Macklin, #950455‐15‐9); Deferoxamine mesylate (DFO, MCE, #HY‐B0988); 3% H 2 O 2 (Lircon, #6926378903443); N‐acetylcysteine (NAC, Sigma, #A7250); Cisplatin (CDDP, Selleck, #S1166). .. Y‐27632 (MCE, #HY‐10071); SMIFH2 (MCE, #HY‐16931); NP‐G2‐044 (MCE, #HY‐125506); Pfn1‐IN‐1 (MCE, #HY‐136808); Benproperine phosphate (MCE, #HY‐114657A); Camalexin (MCE, #HY‐119502); Tetrahydroxyquinone (MCE, #HY‐B1106); Rifamycin S (MCE, #HY‐125365); Nerol (MCE, #HY‐N7063); TrxR‐IN‐5 (MCE, #HY‐147803); Berberine chloride (MCE, #HY‐18258); J14 (MCE, #HY‐135008); CA‐5f (MCE, #HY‐112698); Apocynin (MCE, #HY‐N0088).

    Article Title: ERM Inhibition Confers Ferroptosis Resistance through ROS-Induced NRF2 Signaling.
    Article Snippet: .. NSC305787 (MCE, #HY-18931A) (dissolved in DMSO, sonicated for 5 min to make a 10 m m stock solution, aliquoted and stored at − 80◦C, re-sonicated for 2 min before use); NSC668394 (MCE, #HY-115492); Erastin (Sellcek, #S7242) (dissolved in DMSO to make a 10 m m stock solution, aliquoted and stored at − 80◦C, avoid repeated freeze-thaw cycles); Jasplakinolide (SANTN CRUZ, #102396-24-7); ML385 (TargetMol, #T4360); Zinc Protoporphyrin IX (ZnPP, MCE, #HY-101193); (1S, 3R)-RSL3 (Selleck, #S8155); ML210 (MCE, #HY-100003); Cytochalasin D (CytoD, Glpbio, #GC13440); tert-butyl hydroperoxide (tBOOH, MACKLIN, #B802372-50 mL); 2,3-dimethoxy-1,4naphthalenedione (DMNQ, MCE, #HY-121026); MG-132 (MCE, #HY-13259); Z-VAD (MCE, #HY-16658B); CuCl2 (Macklin, #C804816); Elesclomol (Macklin, #E864529); Ammonium tetrathiomolybdate (TTM, Macklin, #A828261); SB-663825 (MCE, HY-108333); SLK/STK10-IN-1 (MCE, #HY-132868); Chloroquine (CQ, MCE, #HY-17589A); CK-666 (MCE, #HY-16926); Ferrostatin1 (Fer-1, MCE, #HY-100579); Latrunculin A (LatA, Abcam, #ab144290); Brusatol (MCE, #HY-19543); Liproxstatin-1 (Lip1, Macklin, #950455-15-9); Deferoxamine mesylate (DFO, MCE, #HY-B0988); 3% H2 O2 (Lircon, #6926378903443); Nacetylcysteine (NAC, Sigma, #A7250); Cisplatin (CDDP, Selleck, #S1166). .. Y-27632 (MCE, #HY-10071); SMIFH2 (MCE, #HY-16931); NP-G2-044 (MCE, #HY-125506); Pfn1-IN-1 (MCE, #HY-136808); Benproperine phosphate (MCE, #HY-114657A); Camalexin (MCE, #HY-119502); Tetrahydroxyquinone (MCE, #HY-B1106); Rifamycin S (MCE, #HY-125365); Nerol (MCE, #HY-N7063); TrxR-IN-5 (MCE, #HY-147803); Berberine chloride (MCE, #HY-18258); J14 (MCE, #HY-135008); CA-5f (MCE, #HY-112698); Apocynin (MCE, #HY-N0088).

    In Vitro:

    Article Title: G-CSF/NAMPT signaling drives neutrophil dysfunction and enhances bacterial infection susceptibility in cancer patients
    Article Snippet: .. CK‐666 (MedChemExpress), an Arp2/3 complex inhibitor, was dissolved in DMSO and added to the suspensions at a final concentration of 100 μM to inhibit actin branching, based on established in vitro protocols. ..

    Article Title: G-CSF/NAMPT signaling drives neutrophil dysfunction and enhances bacterial infection susceptibility in cancer patients.
    Article Snippet: .. CK‐666 (MedChemExpress), an Arp2/3 complex inhibitor, was dissolved in DMSO and added to the suspensions at a final concentration of 100 μM to inhibit actin branching, based on established in vitro protocols. ..



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    Pharmacological validation and inferred model of US3-mediated actin remodeling. ( a ) Schematic of the machine-learning workflow used to prioritize candidate F-actin regulators. Label-independent quantitative mass-spectrometry features were used for model training, whereas curated actin-regulator annotations were used only to define class labels. Prioritized candidates were subsequently selected for biological interpretation and experimental validation. ( b ) Flow-cytometric quantification of F-actin levels in N2A cells infected with WT HSV-1 or ΔUS3 HSV-1 and treated with the formin inhibitor SMIFH2, the Arp2/3 inhibitor <t>CK-666,</t> or both inhibitors. F-actin abundance was measured as the GeoMean MFI of Alexa Fluor 647–phalloidin at 0 and 24 hpi. Inhibition of either pathway partially attenuated the WT-associated reduction in F-actin, whereas combined inhibition prevented a statistically detectable reduction under the tested conditions. Data represent the mean ± SEM from three independent biological experiments. Statistical significance was assessed using two-way ANOVA followed by Šidák’s multiple-comparisons test. ns, not significant; * p < 0.05; **** p < 0.0001. ( c ) Proposed model integrating the US3 IP-MS interactome, machine-learning-prioritized proteins, and experimentally observed F-actin dynamics. Proteins detected in the US3 IP-MS interactome are distinguished from computationally prioritized or inferred proteins. Arrows represent proposed regulatory relationships, many of which may be indirect. The association between US3 and β-catenin was independently validated by reciprocal co-immunoprecipitation . During early infection, US3 is proposed to promote actin-polymerization programs involving Arp2/3- and formin-associated pathways, potentially supporting intracellular transport. At later stages, US3 is proposed to modulate Rho-family GTPase and cofilin signaling, contributing to stress-fiber disassembly and cytoskeletal remodeling associated with viral egress and spread. Myosin-associated motor complexes may contribute to cytoskeletal organization during both phases.
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    Image Search Results


    Pharmacological validation and inferred model of US3-mediated actin remodeling. ( a ) Schematic of the machine-learning workflow used to prioritize candidate F-actin regulators. Label-independent quantitative mass-spectrometry features were used for model training, whereas curated actin-regulator annotations were used only to define class labels. Prioritized candidates were subsequently selected for biological interpretation and experimental validation. ( b ) Flow-cytometric quantification of F-actin levels in N2A cells infected with WT HSV-1 or ΔUS3 HSV-1 and treated with the formin inhibitor SMIFH2, the Arp2/3 inhibitor CK-666, or both inhibitors. F-actin abundance was measured as the GeoMean MFI of Alexa Fluor 647–phalloidin at 0 and 24 hpi. Inhibition of either pathway partially attenuated the WT-associated reduction in F-actin, whereas combined inhibition prevented a statistically detectable reduction under the tested conditions. Data represent the mean ± SEM from three independent biological experiments. Statistical significance was assessed using two-way ANOVA followed by Šidák’s multiple-comparisons test. ns, not significant; * p < 0.05; **** p < 0.0001. ( c ) Proposed model integrating the US3 IP-MS interactome, machine-learning-prioritized proteins, and experimentally observed F-actin dynamics. Proteins detected in the US3 IP-MS interactome are distinguished from computationally prioritized or inferred proteins. Arrows represent proposed regulatory relationships, many of which may be indirect. The association between US3 and β-catenin was independently validated by reciprocal co-immunoprecipitation . During early infection, US3 is proposed to promote actin-polymerization programs involving Arp2/3- and formin-associated pathways, potentially supporting intracellular transport. At later stages, US3 is proposed to modulate Rho-family GTPase and cofilin signaling, contributing to stress-fiber disassembly and cytoskeletal remodeling associated with viral egress and spread. Myosin-associated motor complexes may contribute to cytoskeletal organization during both phases.

    Journal: Viruses

    Article Title: HSV-1 US3 Hijacks Conserved Actin Regulatory Complexes to Drive F-Actin Remodeling

    doi: 10.3390/v18070793

    Figure Lengend Snippet: Pharmacological validation and inferred model of US3-mediated actin remodeling. ( a ) Schematic of the machine-learning workflow used to prioritize candidate F-actin regulators. Label-independent quantitative mass-spectrometry features were used for model training, whereas curated actin-regulator annotations were used only to define class labels. Prioritized candidates were subsequently selected for biological interpretation and experimental validation. ( b ) Flow-cytometric quantification of F-actin levels in N2A cells infected with WT HSV-1 or ΔUS3 HSV-1 and treated with the formin inhibitor SMIFH2, the Arp2/3 inhibitor CK-666, or both inhibitors. F-actin abundance was measured as the GeoMean MFI of Alexa Fluor 647–phalloidin at 0 and 24 hpi. Inhibition of either pathway partially attenuated the WT-associated reduction in F-actin, whereas combined inhibition prevented a statistically detectable reduction under the tested conditions. Data represent the mean ± SEM from three independent biological experiments. Statistical significance was assessed using two-way ANOVA followed by Šidák’s multiple-comparisons test. ns, not significant; * p < 0.05; **** p < 0.0001. ( c ) Proposed model integrating the US3 IP-MS interactome, machine-learning-prioritized proteins, and experimentally observed F-actin dynamics. Proteins detected in the US3 IP-MS interactome are distinguished from computationally prioritized or inferred proteins. Arrows represent proposed regulatory relationships, many of which may be indirect. The association between US3 and β-catenin was independently validated by reciprocal co-immunoprecipitation . During early infection, US3 is proposed to promote actin-polymerization programs involving Arp2/3- and formin-associated pathways, potentially supporting intracellular transport. At later stages, US3 is proposed to modulate Rho-family GTPase and cofilin signaling, contributing to stress-fiber disassembly and cytoskeletal remodeling associated with viral egress and spread. Myosin-associated motor complexes may contribute to cytoskeletal organization during both phases.

    Article Snippet: Specifically, the formin inhibitor SMIFH2 (MedChemExpress, Monmouth Junction, NJ, USA; 20 μM) and the Arp2/3 complex inhibitor CK-666 (MedChemExpress, Monmouth Junction, NJ, USA;100 μM) were used.

    Techniques: Biomarker Discovery, Mass Spectrometry, Infection, Inhibition, Protein-Protein interactions, Immunoprecipitation

    A549 cells reconstituted with WT-CORO1C or 3KR mutant were treated with DMSO or 100 μM CK-666 for 30 h. A Representative images of phalloidin-stained F-actin (red) in the indicated cell lines treated with DMSO or CK-666. Nuclei are stained with DAPI (blue). Scale bar, 20 μm. CCK-8 proliferation assay ( B ) and clonogenic assay ( C ) of the indicated cell lines treated with DMSO or CK-666. D Quantification of colony numbers from ( C ). E Representative images of Transwell migration (upper) and Matrigel invasion (lower) assays after CK-666 treatment. Scale bar, 50 μm. ( F , G ) Quantitative analysis of migrated and invaded cells from ( E ). H Tumor growth curves of subcutaneous xenografts in mice with or without intraperitoneal injection of CK-666 (20 mg/kg) once a week ( n = 5). I Photographs of dissected tumors from each group at the endpoint ( n = 5). J Final tumor weights in each group. In vivo bioluminescence imaging of orthotopic tumors derived from luciferase-expressing A549 CORO1C WT or 3KR cells in mice with or without intraperitoneal CK-666 treatment. K Representative bioluminescence images. L Quantitative analysis of in vivo radiance signals in ( K ). Data are expressed as means ± SD. M Representative H&E-stained lung sections of metastatic nodules from mice with or without intraperitoneal injection of CK-666 (20 mg/kg) once a week. Arrows indicate metastatic foci. N Quantitative analysis of metastatic foci from ( M ). Quantitative data are expressed as means ± SD.

    Journal: Cell Death & Disease

    Article Title: UBC9-mediated SUMOylation of CORO1C drives lung adenocarcinoma progression via Arp2/3-dependent cytoskeletal remodeling

    doi: 10.1038/s41419-026-08653-w

    Figure Lengend Snippet: A549 cells reconstituted with WT-CORO1C or 3KR mutant were treated with DMSO or 100 μM CK-666 for 30 h. A Representative images of phalloidin-stained F-actin (red) in the indicated cell lines treated with DMSO or CK-666. Nuclei are stained with DAPI (blue). Scale bar, 20 μm. CCK-8 proliferation assay ( B ) and clonogenic assay ( C ) of the indicated cell lines treated with DMSO or CK-666. D Quantification of colony numbers from ( C ). E Representative images of Transwell migration (upper) and Matrigel invasion (lower) assays after CK-666 treatment. Scale bar, 50 μm. ( F , G ) Quantitative analysis of migrated and invaded cells from ( E ). H Tumor growth curves of subcutaneous xenografts in mice with or without intraperitoneal injection of CK-666 (20 mg/kg) once a week ( n = 5). I Photographs of dissected tumors from each group at the endpoint ( n = 5). J Final tumor weights in each group. In vivo bioluminescence imaging of orthotopic tumors derived from luciferase-expressing A549 CORO1C WT or 3KR cells in mice with or without intraperitoneal CK-666 treatment. K Representative bioluminescence images. L Quantitative analysis of in vivo radiance signals in ( K ). Data are expressed as means ± SD. M Representative H&E-stained lung sections of metastatic nodules from mice with or without intraperitoneal injection of CK-666 (20 mg/kg) once a week. Arrows indicate metastatic foci. N Quantitative analysis of metastatic foci from ( M ). Quantitative data are expressed as means ± SD.

    Article Snippet: For pharmacological inhibition of the Arp2/3 complex, cells were treated with CK-666 (MCE, #HY-16926) at a final concentration of 100 μM.

    Techniques: Mutagenesis, Staining, CCK-8 Assay, Proliferation Assay, Clonogenic Assay, Migration, Injection, In Vivo, Imaging, Derivative Assay, Luciferase, Expressing