Adenosine-5'-O-(3-thiotriphosphate) tetralithium salt ≥85% (by HPLC) ATP analog

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An ATP analog that can substitute for ATP in various kinase reactions. The resulting thiophosphorylated proteins are resistant to dephosphorylation by protein phosphatases.

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ICI-118,551 ≥98% (by HPLC)

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Adrenergic receptor ligand.

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25-Hydroxyvitamin D₂ ≥98% (by HPLC)

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High purity vitamin D₂ intermediate.

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(-)-Bicuculline methiodide (synthetic) ≥98% (by HPLC)

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GABAA receptor agonist.

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Phaclofen ≥98% (by HPLC), white solid

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GABAB receptor antagonist.

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AM-404 ≥98% (by TLC)

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Anandamide transport inhibitor

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8-(4-Chlorophenylthio)guanosine 3',5'-cyclic Monophosphothioate, Rp-Isomer triethylammonium salt ≥98% (by HPLC)

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A cell-permeable cGMP antagonist which is resistant to hydrolysis by cyclic nucleotide phosphodiesterases (Ki=0.5 µM). No metabolic side effects. Significantly more lipophilic and membrane permeant as compared to Rp-cGMPS or Rp-8-Br-cGMPS

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AM-630 ≥98% (by TLC)

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Cannabinoid receptor ligand.

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trans-7-Hydroxy-PIPAT maleate ≥98%, white solid

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Dopamine receptor ligand.

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N-(6-Aminohexyl)-5-chloro-1-naphthalenesulphonamide hydrochloride ≥98% (by TLC)

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Binds to calmodulin, inhibiting Ca²⁺-calmodulin-regulated enzyme activity. It inhibits the Ca²⁺/calmodulin-induced activation of myosin light chain kinase in a concentration dependent manner (IC50=25 µM). Cell permeable.

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PK 11195 ≥98% (by TLC)

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Benzodiazepine receptor ligand.

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H-9 HCl ≥98% (by TLC)

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An excellent affinity ligand for chromatographic purification of protein kinases. Inhibits protein kinases (Ki's: PKA=1.9 µM; PKC=18 µM; PKG=0.87 µM; MLCK=70 µM).

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Phloretin ≥98%

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PKC inhibitor

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Erbstatin analog ≥98% (by TLC)

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EGFR inhibitor

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Calyculin A ≥98% (by TLC)

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Inhibitor of PP1 and PP2A

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(±)-Blebbistatin ≥98%

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Inhibitor of non-muscle myosin II

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1,9-Pyrazoloanthrone ≥98% (by TLC)

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Potent, cell permeable, selective, and reversible inhibitor of c-Jun N-terminal kinase (JNK) (IC50=40nM for JNK-1 and JNK-2 and 90nM for JNK-3). The inhibition is competitive with respect to ATP. Exhibits over 300-fold greater selectivity for JNK as compared to ERK1 and p38. Inhibits the phosphorylation of c-Jun and blocks the expression of IL-2, IFN-γ, TNF-α, and COX-2. Blocks IL-1-induced accumulation of phospho-Jun, induction of c-Jun transcription and anti CD3-induced apoptosis of CD4+ CD8+ thymocytes.

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GW 9508 ≥98% (by TLC)

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High potency synthetic agonist at GPR40.

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Eicosapentaenoyl ethanolamide ≥98% (by TLC)

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Eicosapentaenoyl ethanolamide ≥98% (by TLC)

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α-Hydroxyfarnesylphosphonic acid (synthetic) ≥98% (by TLC)

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Potent inhibitor of farnesyltransferase in isolated enzyme assays (IC50=30 nM) and in whole cells. Inhibition of farnesyltransferase is selective over geranylgeranyltransferase I and II (IC50=35.8 µM and 67 µM respectively). α-Hydroxyfarnesylphosphonic acid inhibited (1 µM) Ras processing in Ha-ras-transformed NIH 3T3 fibroblasts.

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AAL-993 ≥98% (by HPLC)

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Highly potent inhibitor of VEGFR-1 (IC50=130nM), VEGFR-2 (IC50=23nM) and VEGFR-3 (IC50=18nM). At higher concentrations it inhibits PDGFR-β (640nM), c-Kit (236nM) and CSF-1R (380nM).