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U 46619

" in MedChemExpress (MCE) Product Catalog:

18

Inhibitors & Agonists

1

Natural
Products

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-108566
    U-46619
    5+ Cited Publications

    9,11-Methanoepoxy PGH2

    		 Prostaglandin Receptor Cardiovascular Disease
    U-46619 (9,11-Methanoepoxy PGH2) is a stable analogue of Thromboxane A2 (HY-113350) (TXA2) and acts as a potent TXA2 (TP) agonist. U-46619 also is a RhoA agonist. U-46619 stimulates the activation of RhoA through TXA2 receptor activation .
    U-46619
  • HY-130356
    5-trans U-46619

    		PGE synthase Others
    5-trans U-46619 is a PGE synthase inhibitor. At a concentration of 10 μM, 5-trans U-46619 inhibits PGE synthase by <20% .
    5-trans U-46619
  • HY-101236
    ICI 192605

    		Prostaglandin Receptor Endocrinology
    ICI 192605 is a potent TXA2R (thromboxane A2 receptor) antagonist as cell signaling prostaglandin. ICI 192605 blocks contraction of isolated guinea pig trachea induced by U-46619 .
    ICI 192605
  • HY-105120A
    Vapiprost hydrochloride

    GR 32191 hydrochloride

    		 Prostaglandin Receptor Others
    Vapiprost hydrochloride (GR 32191 hydrochloride) is a thromboxane A2 receptor antagonist. Vapiprost hydrochloride (GR 32191 hydrochloride) inhibits the aggregation and ATP release stimulated with U-46619, collagen or arachidonic acid (AA) at an IC50 of less than 2.1×10 -8 M .
    Vapiprost hydrochloride
  • HY-105120
    Vapiprost

    GR 32191

    		 Prostaglandin Receptor Others
    Vapiprost (GR 32191) is a thromboxane A2 receptor (TXA2 Receptor) antagonist. Vapiprost hydrochloride (GR 32191 hydrochloride) inhibits the aggregation and ATP release stimulated with U-46619, collagen or arachidonic acid (AA) at an IC50 of less than 2.1×10 -8 M .
    Vapiprost
  • HY-118736
    Ganodermic acid S

    		Others Cardiovascular Disease
    Ganodermic acid S is an oxygenated triterpenoid, that can be isolated from the Chinese medicinal fungus Ganoderma lucidum (Fr.) Karst (Polyporaceae). Ganodermic acid S exerts a concentration dependent inhibition on the response of human gel-filtered platelets (GFP) to U-46619 (HY-108566), a thromboxane (TX) A2 mimetic .
    Ganodermic acid S
  • HY-106105
    ONO 3708

    		Others Others
    ONO 3708 is a TXA2/PGH2 receptor antagonist that can inhibit the binding properties of U46619 in unactivated intact human platelets, with an IC50 value of 38 nM .
    ONO 3708
  • HY-118689
    RA-2

    		Potassium Channel Cardiovascular Disease Neurological Disease Inflammation/Immunology
    RA-2 is a negative-gating modulator of KCa2/3 channels with an IC50 of 17 nM. RA-2 inhibits bradykinin-induced endothelium-derived hyperpolarization (EDH)-type relaxation in U46619-precontracted rings. RA-2 can help to define the physiologic and pathomechanistic roles of KCa2/3 in the vasculature, central nervous system, and during inflammation .
    RA-2
  • HY-137638
    Sp-5,6-DCl-cBIMPS

    		PKA Metabolic Disease
    Sp-5,6-DCl-cBIMPS is a potent and specific cAMP-dependent protein kinases (cAMP-PK) activator. Sp-5,6-DCl-cBIMPS stimulates insulin release. Sp-5,6-DCl-cBIMPS inhibits U46619-induced activation of Rho, Gq and G12/G13 in platelets .
    Sp-5,6-DCl-cBIMPS
  • HY-137638A
    Sp-5,6-DCl-cBIMPS sodium

    Sp-5,6-DCI-cBIMPS

    		 PKA Metabolic Disease
    Sp-5,6-DCl-cBIMPS sodium is a potent and specific cAMP-dependent protein kinases (cAMP-PK) activator. Sp-5,6-DCl-cBIMPS sodium stimulates insulin release. Sp-5,6-DCl-cBIMPS sodium inhibits U-46619 (HY-108566)-induced activation of Rho, Gq and G12/G13 in platelets .
    Sp-5,6-DCl-cBIMPS sodium
  • HY-101390
    (+)-Niguldipine hydrochloride

    (S)-Niguldipine hydrochloride

    		 Calcium Channel Cardiovascular Disease
    (+)-Niguldipine hydrochloride is an antagonist for calcium channel. (+)-Niguldipine hydrochloride produces vasodilation by blocking calcium channels and reducing the transmembrane influx of calcium ions. (+)-Niguldipine hydrochloride inhibits U-46619 (HY-108566)-induced coronary vasoconstriction in guinea pig Langendorff heart with pID50 of 11.37, binds to calcium channel on guinea pig skeletal muscle membrane with Ki of 9.75, and lowers the blood pressure in spontaneously hypertensive rat with pED30 of 7.1. (+)-Niguldipine hydrochloride ameliorates cardiovascular diseases such as hypertension, angina pectoris and arrhythmias .
    (+)-Niguldipine hydrochloride
  • HY-129851
    NTP42

    		Prostaglandin Receptor Cardiovascular Disease
    NTP42 is a thromboxane A2 (TXA2) receptor antagonist with an IC50 of 3.278 nM for antagonizing T prostanoid receptor (TP)- mediated [Ca 2+] mobilization following stimulation of cells with the alternative TP agonist U46619 . NTP42 can be used for the treatment of pulmonary arterial hypertension (PAH) .
    NTP42
  • HY-101390A
    (-)-Niguldipine hydrochloride

    (R)-Niguldipine hydrochloride

    		 Calcium Channel Cardiovascular Disease
    (-)-Niguldipine ((R)-Niguldipine) hydrochloride is a calcium channel antagonist. (-)-Niguldipine hydrochloride exerts a vasodilatory effect by blocking calcium channels and reducing the transmembrane influx of calcium ions. (-)-Niguldipine can inhibit U-46619 (HY-108566)-induced coronary artery contraction in guinea pig Langendorff hearts (pID50 of 9.93), has high affinity for calcium channel binding sites on guinea pig skeletal muscle membranes (Ki of 8.10), and lowers blood pressure in spontaneously hypertensive rats (pED30 of 5.55). (-)-Niguldipine hydrochloride can improve cardiovascular diseases such as hypertension, angina pectoris, and arrhythmias .
    (-)-Niguldipine hydrochloride
  • HY-117044A
    (±)12-HEPE

    		Others Metabolic Disease
    (±)12-HEPE is produced by non-enzymatic oxidation of EPA. It contains equal amounts of 12(S)-HEPE and 12(R)-HEPE. The biological activity of (±)12-HEPE is likely mediated by one of the individual isomers, most commonly the 12(S) isomer in mammalian systems. 12-HEPE inhibits platelet aggregation with the same potency as 12-HETE, exhibiting IC50 values of 24 and 25 μM, respectively.1 These compounds are also equipotent as inhibitors of U46619-induced contraction of rat aorta (IC50s=8.6-8.8 μM).
    (±)12-HEPE
  • HY-78263
    MNS

    NSC 170724; 5-(2-Nitrovinyl)benzodioxole

    		 Src Syk Cancer
    MNS (NSC 170724), the beta-nitrostyrene derivative, is a potent tyrosine kinase inhibitor and a broad-spectrum antiplatelet agent. MNS completely inhibits U46619, ADP-, arachidonic acid-, collagen-, and thrombin-induced platelet aggregation with IC50 values of 2.1, 4.1, 5.8, 7.0, and 12.7 μM, respectively. MNS inhibits Src, Syk, and FAK with IC50 of 27.3, 2.8, and 97.6 μM, respectively .
    MNS
  • HY-108556A
    RWJ-56110 dihydrochloride

    		Protease Activated Receptor (PAR) Apoptosis Cardiovascular Disease
    RWJ-56110 dihydrochloride is a potent, selective, peptide-mimetic inhibitor of PAR-1 activation and internalization (binding IC50=0.44 uM) and shows no effect on PAR-2, PAR-3, or PAR-4. RWJ-56110 dihydrochloride inhibits the aggregation of human platelets induced by?both?SFLLRN-NH2?(IC50=0.16 μM) and thrombin (IC50=0.34 μM), quite selective?relative to U46619 (HY-108566). RWJ-56110 dihydrochloride blocks angiogenesis and blocks the formation of new vessels in vivo. RWJ-56110 dihydrochloride induces cell apoptosis .
    RWJ-56110 dihydrochloride
  • HY-108556
    RWJ-56110

    		Protease Activated Receptor (PAR) Apoptosis Cardiovascular Disease
    RWJ-56110 is a potent, selective, peptide-mimetic inhibitor of PAR-1 activation and internalization (binding IC50=0.44 uM) and shows no effect on PAR-2, PAR-3, or PAR-4. RWJ-56110 inhibits the aggregation of human platelets induced by?both?SFLLRN-NH2?(IC50=0.16 μM) and thrombin (IC50=0.34 μM), quite selective?relative to U46619 (HY-108566). RWJ-56110 inhibits angiogenesis and blocks the formation of new vessels in vivo. RWJ-56110 induces cell apoptosis .
    RWJ-56110
  • HY-113884
    (R)-Coriolic acid

    13(R)-HODE

    		 Endogenous Metabolite Metabolic Disease
    13(R)-HODE is the opposite enantiomer of the 13(S)-HODE produced when linoleic acid is incubated with soybean lipoxygenase. The presence of 13(R)-HODE in the supernatants and membranes of cultured bovine endothelial cells has been attributed to COX metabolism.1 13(R)-HODE is a weak (IC50=2.7 μM) inhibitor of U-46619-induced platelet aggregation.
    (R)-Coriolic acid

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