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calphostin  (Tocris)


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    Tocris calphostin
    Calphostin, supplied by Tocris, used in various techniques. Bioz Stars score: 95/100, based on 103 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/calphostin+c/AR-C+118925XX/pm39863058-59-2-10
    Average 95 stars, based on 103 article reviews
    calphostin - by Bioz Stars, 2026-09
    95/100 stars

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    other:

    Article Title: Platelet-derived growth factor (PDGF)-BB regulates the airway tone via activation of MAP2K, thromboxane, actin polymerisation and Ca 2+ -sensitisation
    Article Snippet: Imatinib mesylate, amlodipine, fasudile, calphostin C, SC51322, PF04418948, L798106 and L161982 were purchased from Tocris Bioscience (Ellisville, Missouri, USA).

    Article Title: Inflammatory Stimulation Upregulates the Receptor Transporter Protein 4 (RTP4) in SIM-A9 Microglial Cells
    Article Snippet: The following reagents were used: Lipopolyssaccharide (LPS) (Sigma-Aldrich, St. Louis, MO, USA), Calphostin C, an inhibitor of protein kinase C (PKC) (Tocris, Bio-Techne Japan, Tokyo, Japan), U0126, a potent, selective inhibitor of MEK1 and 2 (Tocris, Bio-Techne Japan, Tokyo, Japan), Pyridone 6, a potent pan-JAK inhibitor (Tocris, Bio-Techne Japan, Tokyo, Japan), TAK242, a selective Toll-like receptor 4 (TLR4) inhibitor (Merk, Japan).

    Article Title: Inflammatory Stimulation Upregulates the Receptor Transporter Protein 4 (RTP4) in SIM-A9 Microglial Cells.
    Article Snippet: The following reagents were used: Lipopolyssaccharide (LPS) (Sigma-Aldrich, St. Louis, MO, USA), Calphostin C, an inhibitor of protein kinase C (PKC) (Tocris, Bio-Techne Japan, Tokyo, Japan), U0126, a potent, selective inhibitor of MEK1 and 2 (Tocris, Bio-Techne Japan, Tokyo, Japan), Pyridone 6, a potent pan-JAK inhibitor (Tocris, Bio-Techne Japan, Tokyo, Japan), TAK242, a selective Toll-like receptor 4 (TLR4) inhibitor (Merk, Japan).

    Cell Culture:

    Article Title: Microvesicles from stored red blood cells induce P-selectin and von Willebrand factor release from endothelial cells via a protein kinase C-dependent mechanism.
    Article Snippet: 8-Bromo-cAMP is a PKA activator (R&D Systems, Minneapolis, MN) and phorbol 12-myristate 13-acetate (PMA) is a PKC activator (Abcam, Cambridge, UK) which were both utilized in cell culture experiments (8-Bromo-cAMP: 100 μM, 1 mM; PMA: 1 μM). .. PKI 14–22 amide (R&D Systems, Minneapolis, MN) is a PKA inhibitor and calphostin C (Tocris Bioscience, Minneapolis, MN) is a PKC inhibitor which were both used in cell culture experiments (PKI 14–22: 10 μM; calphostin C: 10 μg/mL). ..

    Recombinant:

    Article Title: The P2Y 11 receptor of human M2 macrophages activates canonical and IL-1 receptor signaling to translate the extracellular danger signal ATP into anti-inflammatory and pro-angiogenic responses.
    Article Snippet: The slowly hydrolyzable ATP analog ATPγS [7, 20] (Sigma Aldrich, St. Louis, MO, USA) as well as the suramin analog NF340 [7, 10, 13, 21] (Santa Cruz, Dallas, TX, USA) served as P2Y11 receptor agonist (20 μM) and antagonist (20 μM), respectively. .. Further reagents utilized in this study include the PDE4-selective inhibitor rolipram (10 μM) (SigmaAldrich), BAPTA-AM (10 μM) (Sigma-Aldrich), calphostin C (250 nM) (Tocris), recombinant IL-1α and IL-1β (0.5–2 ng·ml−1) (R&D Systems, Minneapolis, MN, USA), the TACE/ADAM17 inhibitor TAPI-1 (20 μM) (Tocris), the selective inhibitor of Epac1 (R)-CE3F4 (20 μM) (Tocris), and the humanized anti-VEGF monoclonal antibody bevacizumab (0.5 μg ml−1) (Selleckchem, Houston, TX, USA). ..

    Article Title: The P2Y 11 receptor of human M2 macrophages activates canonical and IL-1 receptor signaling to translate the extracellular danger signal ATP into anti-inflammatory and pro-angiogenic responses
    Article Snippet: The slowly hydrolyzable ATP analog ATPγS [ , ] (Sigma Aldrich, St. Louis, MO, USA) as well as the suramin analog NF340 [ , , , ] (Santa Cruz, Dallas, TX, USA) served as P2Y 11 receptor agonist (20 μM) and antagonist (20 μM), respectively. .. Further reagents utilized in this study include the PDE4-selective inhibitor rolipram (10 μM) (Sigma-Aldrich), BAPTA-AM (10 μM) (Sigma-Aldrich), calphostin C (250 nM) (Tocris), recombinant IL-1α and IL-1β (0.5–2 ng·ml −1 ) (R&D Systems, Minneapolis, MN, USA), the TACE/ADAM17 inhibitor TAPI-1 (20 μM) (Tocris), the selective inhibitor of Epac1 (R)-CE3F4 (20 μM) (Tocris), and the humanized anti-VEGF monoclonal antibody bevacizumab (0.5 μg ml −1 ) (Selleckchem, Houston, TX, USA). ..

    Concentration Assay:

    Article Title: Interferon-γ enhances neocortical synaptic inhibition by promoting membrane association and phosphorylation of GABA A receptors in a protein kinase C-dependent manner.
    Article Snippet: Interferon-γ (IFN-γ), an important mediator of the antiviral immune response, can also act as a neuromodulator.. CNS IFN-γ levels rise acutely in response to infection and therapeutically applied IFN-γ provokes CNS related side effects.. Moreover, IFN-γ plays a key role in neurophysiological processes and a variety of chronic neurological and neuropsychiatric conditions.



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    calphostin c  (MedChemExpress)
    94
    MedChemExpress calphostin c
    ( A ) Schematic of the metastasis functional screening using molecular inhibitors in vivo. ( B, C, and D ) Gross pulmonary metastases from human melanoma A375sm (B), mouse melanoma B16F10 (C), and mouse rhabdomyosarcoma RMS14 (D) in response to molecular inhibitor in the experimental metastasis assay by tail vein injection. Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). Cal C, 100 nM calphostin C; Rho, 12nM Rho Inhibitor I; Rap, 10nM Rapamycin; H-89, 50nM PKA inhibitor; SB, 10µM p38 inhibitor SB203580; TSA, 300nM HDAC inhibitor Trichostatin A; MS, 10µM HDAC inhibitor MS-275; PD, 20µM MAPK inhibitor PD98059; LY, 10µM PI3K/AKT inhibitor LY294002. ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n = 10. ( E, F, and G ) The related cell viability of human melanoma A375sm (E), mouse melanoma B16F10 (F), and mouse rhabdomyosarcoma (G) cells, pretreated with molecular inhibitors. Data are represented as mean ± SEM of three independent experiments. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. ( H ) Gross pulmonary metastases from mouse melanoma B16F10 pretreated with 10µM PI3K/AKT inhibitor LY294002 at the indicated time (LY12, 12 hours, LY24, 24 hours and LY48, 48 hours). Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n=10. ( I ) Gross pulmonary metastases from mouse rhabdomyosarcoma RMS14 cells pretreated with 20µM MAPK inhibitor PD98059 at the indicated time (PD12, 12 hours, PD24, 24 hours and PD48, 48 hours). Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n=10.
    Calphostin C, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/calphostin+c/Calphostin+C/bio_rxiv__64898__2026__02__07__704548-178-0-40
    Average 94 stars, based on 1 article reviews
    calphostin c - by Bioz Stars, 2026-09
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    calphostin  (Tocris)
    95
    Tocris calphostin
    ( A ) Schematic of the metastasis functional screening using molecular inhibitors in vivo. ( B, C, and D ) Gross pulmonary metastases from human melanoma A375sm (B), mouse melanoma B16F10 (C), and mouse rhabdomyosarcoma RMS14 (D) in response to molecular inhibitor in the experimental metastasis assay by tail vein injection. Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). Cal C, 100 nM calphostin C; Rho, 12nM Rho Inhibitor I; Rap, 10nM Rapamycin; H-89, 50nM PKA inhibitor; SB, 10µM p38 inhibitor SB203580; TSA, 300nM HDAC inhibitor Trichostatin A; MS, 10µM HDAC inhibitor MS-275; PD, 20µM MAPK inhibitor PD98059; LY, 10µM PI3K/AKT inhibitor LY294002. ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n = 10. ( E, F, and G ) The related cell viability of human melanoma A375sm (E), mouse melanoma B16F10 (F), and mouse rhabdomyosarcoma (G) cells, pretreated with molecular inhibitors. Data are represented as mean ± SEM of three independent experiments. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. ( H ) Gross pulmonary metastases from mouse melanoma B16F10 pretreated with 10µM PI3K/AKT inhibitor LY294002 at the indicated time (LY12, 12 hours, LY24, 24 hours and LY48, 48 hours). Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n=10. ( I ) Gross pulmonary metastases from mouse rhabdomyosarcoma RMS14 cells pretreated with 20µM MAPK inhibitor PD98059 at the indicated time (PD12, 12 hours, PD24, 24 hours and PD48, 48 hours). Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n=10.
    Calphostin, supplied by Tocris, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/calphostin+c/AR-C+118925XX/pm39863058-59-2-10
    Average 95 stars, based on 1 article reviews
    calphostin - by Bioz Stars, 2026-09
    95/100 stars
    		  Buy from Supplier
    calphostin c  (Tocris)
    93
    Tocris calphostin c
    ( A ) Schematic of the metastasis functional screening using molecular inhibitors in vivo. ( B, C, and D ) Gross pulmonary metastases from human melanoma A375sm (B), mouse melanoma B16F10 (C), and mouse rhabdomyosarcoma RMS14 (D) in response to molecular inhibitor in the experimental metastasis assay by tail vein injection. Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). Cal C, 100 nM calphostin C; Rho, 12nM Rho Inhibitor I; Rap, 10nM Rapamycin; H-89, 50nM PKA inhibitor; SB, 10µM p38 inhibitor SB203580; TSA, 300nM HDAC inhibitor Trichostatin A; MS, 10µM HDAC inhibitor MS-275; PD, 20µM MAPK inhibitor PD98059; LY, 10µM PI3K/AKT inhibitor LY294002. ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n = 10. ( E, F, and G ) The related cell viability of human melanoma A375sm (E), mouse melanoma B16F10 (F), and mouse rhabdomyosarcoma (G) cells, pretreated with molecular inhibitors. Data are represented as mean ± SEM of three independent experiments. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. ( H ) Gross pulmonary metastases from mouse melanoma B16F10 pretreated with 10µM PI3K/AKT inhibitor LY294002 at the indicated time (LY12, 12 hours, LY24, 24 hours and LY48, 48 hours). Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n=10. ( I ) Gross pulmonary metastases from mouse rhabdomyosarcoma RMS14 cells pretreated with 20µM MAPK inhibitor PD98059 at the indicated time (PD12, 12 hours, PD24, 24 hours and PD48, 48 hours). Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n=10.
    Calphostin C, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/calphostin+c/Calphostin+C/pm39769444-286-12-21
    Average 93 stars, based on 1 article reviews
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    calphostin c  (Adipogen)
    90
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    ( A ) Schematic of the metastasis functional screening using molecular inhibitors in vivo. ( B, C, and D ) Gross pulmonary metastases from human melanoma A375sm (B), mouse melanoma B16F10 (C), and mouse rhabdomyosarcoma RMS14 (D) in response to molecular inhibitor in the experimental metastasis assay by tail vein injection. Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). Cal C, 100 nM calphostin C; Rho, 12nM Rho Inhibitor I; Rap, 10nM Rapamycin; H-89, 50nM PKA inhibitor; SB, 10µM p38 inhibitor SB203580; TSA, 300nM HDAC inhibitor Trichostatin A; MS, 10µM HDAC inhibitor MS-275; PD, 20µM MAPK inhibitor PD98059; LY, 10µM PI3K/AKT inhibitor LY294002. ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n = 10. ( E, F, and G ) The related cell viability of human melanoma A375sm (E), mouse melanoma B16F10 (F), and mouse rhabdomyosarcoma (G) cells, pretreated with molecular inhibitors. Data are represented as mean ± SEM of three independent experiments. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. ( H ) Gross pulmonary metastases from mouse melanoma B16F10 pretreated with 10µM PI3K/AKT inhibitor LY294002 at the indicated time (LY12, 12 hours, LY24, 24 hours and LY48, 48 hours). Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n=10. ( I ) Gross pulmonary metastases from mouse rhabdomyosarcoma RMS14 cells pretreated with 20µM MAPK inhibitor PD98059 at the indicated time (PD12, 12 hours, PD24, 24 hours and PD48, 48 hours). Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n=10.
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    https://www.bioz.com/product/calphostin+c/calphostin+c/pm39368603-51-0-7
    Average 90 stars, based on 1 article reviews
    calphostin c - by Bioz Stars, 2026-09
    90/100 stars
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    calphostin c  (Cayman Chemical)
    90
    Cayman Chemical calphostin c
    ( A ) Schematic of the metastasis functional screening using molecular inhibitors in vivo. ( B, C, and D ) Gross pulmonary metastases from human melanoma A375sm (B), mouse melanoma B16F10 (C), and mouse rhabdomyosarcoma RMS14 (D) in response to molecular inhibitor in the experimental metastasis assay by tail vein injection. Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). Cal C, 100 nM calphostin C; Rho, 12nM Rho Inhibitor I; Rap, 10nM Rapamycin; H-89, 50nM PKA inhibitor; SB, 10µM p38 inhibitor SB203580; TSA, 300nM HDAC inhibitor Trichostatin A; MS, 10µM HDAC inhibitor MS-275; PD, 20µM MAPK inhibitor PD98059; LY, 10µM PI3K/AKT inhibitor LY294002. ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n = 10. ( E, F, and G ) The related cell viability of human melanoma A375sm (E), mouse melanoma B16F10 (F), and mouse rhabdomyosarcoma (G) cells, pretreated with molecular inhibitors. Data are represented as mean ± SEM of three independent experiments. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. ( H ) Gross pulmonary metastases from mouse melanoma B16F10 pretreated with 10µM PI3K/AKT inhibitor LY294002 at the indicated time (LY12, 12 hours, LY24, 24 hours and LY48, 48 hours). Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n=10. ( I ) Gross pulmonary metastases from mouse rhabdomyosarcoma RMS14 cells pretreated with 20µM MAPK inhibitor PD98059 at the indicated time (PD12, 12 hours, PD24, 24 hours and PD48, 48 hours). Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n=10.
    Calphostin C, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/calphostin+c/calphostin+c/pmc11872787__ALR___15___287___s001-8-0-16
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    calphostin c - by Bioz Stars, 2026-09
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    calphostin c hb0160  (Hello Bio Inc)
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    Hello Bio Inc calphostin c hb0160
    ( A ) Schematic of the metastasis functional screening using molecular inhibitors in vivo. ( B, C, and D ) Gross pulmonary metastases from human melanoma A375sm (B), mouse melanoma B16F10 (C), and mouse rhabdomyosarcoma RMS14 (D) in response to molecular inhibitor in the experimental metastasis assay by tail vein injection. Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). Cal C, 100 nM calphostin C; Rho, 12nM Rho Inhibitor I; Rap, 10nM Rapamycin; H-89, 50nM PKA inhibitor; SB, 10µM p38 inhibitor SB203580; TSA, 300nM HDAC inhibitor Trichostatin A; MS, 10µM HDAC inhibitor MS-275; PD, 20µM MAPK inhibitor PD98059; LY, 10µM PI3K/AKT inhibitor LY294002. ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n = 10. ( E, F, and G ) The related cell viability of human melanoma A375sm (E), mouse melanoma B16F10 (F), and mouse rhabdomyosarcoma (G) cells, pretreated with molecular inhibitors. Data are represented as mean ± SEM of three independent experiments. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. ( H ) Gross pulmonary metastases from mouse melanoma B16F10 pretreated with 10µM PI3K/AKT inhibitor LY294002 at the indicated time (LY12, 12 hours, LY24, 24 hours and LY48, 48 hours). Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n=10. ( I ) Gross pulmonary metastases from mouse rhabdomyosarcoma RMS14 cells pretreated with 20µM MAPK inhibitor PD98059 at the indicated time (PD12, 12 hours, PD24, 24 hours and PD48, 48 hours). Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n=10.
    Calphostin C Hb0160, supplied by Hello Bio Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/calphostin+c/calphostin+c/10__1113_slash_jp284845-213-0-4
    Average 90 stars, based on 1 article reviews
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    pkc inhibitor, calphostin c  (Cayman Chemical)
    90
    Cayman Chemical pkc inhibitor, calphostin c
    ( A ) Schematic of the metastasis functional screening using molecular inhibitors in vivo. ( B, C, and D ) Gross pulmonary metastases from human melanoma A375sm (B), mouse melanoma B16F10 (C), and mouse rhabdomyosarcoma RMS14 (D) in response to molecular inhibitor in the experimental metastasis assay by tail vein injection. Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). Cal C, 100 nM calphostin C; Rho, 12nM Rho Inhibitor I; Rap, 10nM Rapamycin; H-89, 50nM PKA inhibitor; SB, 10µM p38 inhibitor SB203580; TSA, 300nM HDAC inhibitor Trichostatin A; MS, 10µM HDAC inhibitor MS-275; PD, 20µM MAPK inhibitor PD98059; LY, 10µM PI3K/AKT inhibitor LY294002. ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n = 10. ( E, F, and G ) The related cell viability of human melanoma A375sm (E), mouse melanoma B16F10 (F), and mouse rhabdomyosarcoma (G) cells, pretreated with molecular inhibitors. Data are represented as mean ± SEM of three independent experiments. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. ( H ) Gross pulmonary metastases from mouse melanoma B16F10 pretreated with 10µM PI3K/AKT inhibitor LY294002 at the indicated time (LY12, 12 hours, LY24, 24 hours and LY48, 48 hours). Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n=10. ( I ) Gross pulmonary metastases from mouse rhabdomyosarcoma RMS14 cells pretreated with 20µM MAPK inhibitor PD98059 at the indicated time (PD12, 12 hours, PD24, 24 hours and PD48, 48 hours). Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n=10.
    Pkc Inhibitor, Calphostin C, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/calphostin+c/pkc+inhibitor++calphostin+c/pmc11042806-146-2-8
    Average 90 stars, based on 1 article reviews
    pkc inhibitor, calphostin c - by Bioz Stars, 2026-09
    90/100 stars
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    Image Search Results


    ( A ) Schematic of the metastasis functional screening using molecular inhibitors in vivo. ( B, C, and D ) Gross pulmonary metastases from human melanoma A375sm (B), mouse melanoma B16F10 (C), and mouse rhabdomyosarcoma RMS14 (D) in response to molecular inhibitor in the experimental metastasis assay by tail vein injection. Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). Cal C, 100 nM calphostin C; Rho, 12nM Rho Inhibitor I; Rap, 10nM Rapamycin; H-89, 50nM PKA inhibitor; SB, 10µM p38 inhibitor SB203580; TSA, 300nM HDAC inhibitor Trichostatin A; MS, 10µM HDAC inhibitor MS-275; PD, 20µM MAPK inhibitor PD98059; LY, 10µM PI3K/AKT inhibitor LY294002. ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n = 10. ( E, F, and G ) The related cell viability of human melanoma A375sm (E), mouse melanoma B16F10 (F), and mouse rhabdomyosarcoma (G) cells, pretreated with molecular inhibitors. Data are represented as mean ± SEM of three independent experiments. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. ( H ) Gross pulmonary metastases from mouse melanoma B16F10 pretreated with 10µM PI3K/AKT inhibitor LY294002 at the indicated time (LY12, 12 hours, LY24, 24 hours and LY48, 48 hours). Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n=10. ( I ) Gross pulmonary metastases from mouse rhabdomyosarcoma RMS14 cells pretreated with 20µM MAPK inhibitor PD98059 at the indicated time (PD12, 12 hours, PD24, 24 hours and PD48, 48 hours). Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n=10.

    Journal: bioRxiv

    Article Title: Targeting one-carbon metabolic vulnerabilities of metastasis with therapeutic potential

    doi: 10.64898/2026.02.07.704548

    Figure Lengend Snippet: ( A ) Schematic of the metastasis functional screening using molecular inhibitors in vivo. ( B, C, and D ) Gross pulmonary metastases from human melanoma A375sm (B), mouse melanoma B16F10 (C), and mouse rhabdomyosarcoma RMS14 (D) in response to molecular inhibitor in the experimental metastasis assay by tail vein injection. Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). Cal C, 100 nM calphostin C; Rho, 12nM Rho Inhibitor I; Rap, 10nM Rapamycin; H-89, 50nM PKA inhibitor; SB, 10µM p38 inhibitor SB203580; TSA, 300nM HDAC inhibitor Trichostatin A; MS, 10µM HDAC inhibitor MS-275; PD, 20µM MAPK inhibitor PD98059; LY, 10µM PI3K/AKT inhibitor LY294002. ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n = 10. ( E, F, and G ) The related cell viability of human melanoma A375sm (E), mouse melanoma B16F10 (F), and mouse rhabdomyosarcoma (G) cells, pretreated with molecular inhibitors. Data are represented as mean ± SEM of three independent experiments. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. ( H ) Gross pulmonary metastases from mouse melanoma B16F10 pretreated with 10µM PI3K/AKT inhibitor LY294002 at the indicated time (LY12, 12 hours, LY24, 24 hours and LY48, 48 hours). Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n=10. ( I ) Gross pulmonary metastases from mouse rhabdomyosarcoma RMS14 cells pretreated with 20µM MAPK inhibitor PD98059 at the indicated time (PD12, 12 hours, PD24, 24 hours and PD48, 48 hours). Data are represented as mean ± SEM. The p-values were presented from an unpaired t-test analysis (two-tailed) compared with the control (DMSO). ND , no statistical difference; * p < 0.05; ** p < 0.01; *** p < 0.001. n=10.

    Article Snippet: Calphostin C, Rho Inhibitor I, Rapamycin, PKA inhibitor H-89, p38 inhibitor SB203580, HADC inhibitor Trichostatin A and MS-275, MAPK inhibitor PD98059, PI3K/AKT inhibitor LY294002, Rottlerin, bisindoylmaleimide I (BMI), PKC β inhibitor I, and FDA-approved-Drug-Library (1562 compounds, HY-L022) were obtained from MedChemExpress (Monmouth Junction, NJ).

    Techniques: Functional Assay, In Vivo, Injection, Two Tailed Test, Control

    (A) Schematic of microarray analysis to focus on the inhibition of tumor metastasis. (B) The significant differentiated gene expression patterns associated with the inhibition of tumor metastasis progression and the identification of metabolism pathways associated with tumor metastasis. The significantly expressed genes in B16F10 (a) or RMS14 (b) cells treated with inhibitors (Cal C, 100 nM calphostin; Rap, 10nM Rapamycin; 20µM MAPK inhibitor PD98059; LY, 10µM PI3K/AKT inhibitor LY294002) compared with DMSO control were filtered by a p-value of 0.05 and an absolute value of fold change of 1.5 in ANOVA analysis. a1, Cal C v.s. DMSO; a2, Rap v.s. DMSO; a3, LY24 v.s. DMSO; a4, LY48 v.s. DMSO in B16F10 cells. b1, Cal C v.s. DMSO; b2, Rap v.s. DMSO; b3, PD24 v.s. DMSO; b4, PD48 v.s. DMSO in RMS14 cells. ( C ) Gene signaling pathway (GO gene pathway) analysis revealed that top 15 biological pathways and functions within a given gene list from micrroarry analysis regulate one-carbon metabolism and de novo serine synthesis (SSP). Both p and FDR valuest were transformed to negative log (-log2) values. ( D ) Schematic of the one-carbon metabolism and De novo serine synthesis (SSP) pathways. ( E to H ) Validation of gene expression identified in cDNA microarray analysis by Western blot analysis. The human melanoma A375sm (E) and WM88 (F), mouse melanoma B16F10 (G), or mouse rhabdomyosarcoma RMS14 (H) cells were treated with molecular inhibitors. DMSO, as a mock control; Cal C, 100 nM calphostin C; Rho, 12nM Rho Inhibitor I; Rap, 10nM Rapamycin; SB, 10 µM p38 inhibitor SB203580; PD, 20 µM MAPK inhibitor PD98059; LY, 10 µM PI3K/AKT inhibitor LY294002; Rott, 5μM of rottlerin; BMI, 20 nM of bisindoylmaleimide I; Iβ, 20 nM of PKCβ inhibitor I. β -actin was used as a control.

    Journal: bioRxiv

    Article Title: Targeting one-carbon metabolic vulnerabilities of metastasis with therapeutic potential

    doi: 10.64898/2026.02.07.704548

    Figure Lengend Snippet: (A) Schematic of microarray analysis to focus on the inhibition of tumor metastasis. (B) The significant differentiated gene expression patterns associated with the inhibition of tumor metastasis progression and the identification of metabolism pathways associated with tumor metastasis. The significantly expressed genes in B16F10 (a) or RMS14 (b) cells treated with inhibitors (Cal C, 100 nM calphostin; Rap, 10nM Rapamycin; 20µM MAPK inhibitor PD98059; LY, 10µM PI3K/AKT inhibitor LY294002) compared with DMSO control were filtered by a p-value of 0.05 and an absolute value of fold change of 1.5 in ANOVA analysis. a1, Cal C v.s. DMSO; a2, Rap v.s. DMSO; a3, LY24 v.s. DMSO; a4, LY48 v.s. DMSO in B16F10 cells. b1, Cal C v.s. DMSO; b2, Rap v.s. DMSO; b3, PD24 v.s. DMSO; b4, PD48 v.s. DMSO in RMS14 cells. ( C ) Gene signaling pathway (GO gene pathway) analysis revealed that top 15 biological pathways and functions within a given gene list from micrroarry analysis regulate one-carbon metabolism and de novo serine synthesis (SSP). Both p and FDR valuest were transformed to negative log (-log2) values. ( D ) Schematic of the one-carbon metabolism and De novo serine synthesis (SSP) pathways. ( E to H ) Validation of gene expression identified in cDNA microarray analysis by Western blot analysis. The human melanoma A375sm (E) and WM88 (F), mouse melanoma B16F10 (G), or mouse rhabdomyosarcoma RMS14 (H) cells were treated with molecular inhibitors. DMSO, as a mock control; Cal C, 100 nM calphostin C; Rho, 12nM Rho Inhibitor I; Rap, 10nM Rapamycin; SB, 10 µM p38 inhibitor SB203580; PD, 20 µM MAPK inhibitor PD98059; LY, 10 µM PI3K/AKT inhibitor LY294002; Rott, 5μM of rottlerin; BMI, 20 nM of bisindoylmaleimide I; Iβ, 20 nM of PKCβ inhibitor I. β -actin was used as a control.

    Article Snippet: Calphostin C, Rho Inhibitor I, Rapamycin, PKA inhibitor H-89, p38 inhibitor SB203580, HADC inhibitor Trichostatin A and MS-275, MAPK inhibitor PD98059, PI3K/AKT inhibitor LY294002, Rottlerin, bisindoylmaleimide I (BMI), PKC β inhibitor I, and FDA-approved-Drug-Library (1562 compounds, HY-L022) were obtained from MedChemExpress (Monmouth Junction, NJ).

    Techniques: Microarray, Inhibition, Gene Expression, Control, Transformation Assay, Biomarker Discovery, Western Blot