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You are here:Home-Inhibitors & Agonists-Immunology/Inflammation-Nitric Oxide Synthase (NOS)

Request The Product List ofNitric Oxide Synthase (NOS) Nitric Oxide Synthase (NOS)

Nitric oxide synthases (NOSs) are a family of enzymes catalyzing the production of nitric oxide (NO) from L-arginine. NO synthases catalyze the oxidation of L-arginine to NO and L-citrulline. Mammals contain three NOS isoforms: neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS). NO produced from these different NOS isoforms is involved in a wide range of physiologic functions in the nervous, immune, and cardiovascular systems. Unregulated NO production can lead to pathologic conditions such as stroke, inflammation, and hypertension. Therefore, the control of NOS activity by isoform selective NOS inhibitors has great potential for therapeutic treatments of NO-related diseases.

Cat. No. Product Name CAS No. Information
GY10094

ZLc002

ZLc002 (ZLc-002) is a putative small-molecule inhibitor of nNOS interaction with NOS1AP, disrupts neuronal nitric oxide synthase-NOS1AP interaction in intact cells; exhibits anxiolytic-like efficacy in a mouse model of chronic mild stress without altering appetite, general activity, or locomotor activity or interfering with the resting potential of neurons, also inhibits co-immunoprecipitation of NOS1AP with nNOS in hippocampal cells; suppresses inflammatory nociception and chemotherapy-induced neuropathic pain and synergizes with paclitaxel to reduce tumor cell viability; suppresses formalin-evoked inflammatory pain in rats and reduced Fos protein-like immunoreactivity in the lumbar spinal dorsal horn (4-10 mg/kg i.p.).

GY06668

ZL-006

1181226-02-7

ZL-006 (ZL 006, ZL006) is a brain penetrant small molecule inhibitor of PSD-95/nNOS interaction that prevents glutamate-induced excitotoxicity and cerebral ischemic damage in vivo; selectively blocks the ischemia-induced nNOS-PSD-95 association, shows potent neuroprotective activity in vitro and ameliorates focal cerebral ischemic damage in mice and rats subjected to middle cerebral artery occlusion (MCAO) and reperfusio; does not inhibit NMDAR function, catalytic activity of nNOS or spatial memory, and has no effect on aggressive behaviors.

GY06661

BYK191023 dihydrochloride

1216722-25-6

BYK191023 dihydrochloride (BYK-191023) is a potent, highly selective inhibitor of inducible nitric-oxide synthase (iNOS) with IC50 of 86 nM, >20-fold selectivity over nNOS and eNOS (IC50=17 and 162 uM); exhibits an affinity for iNOS, nNOS, and eNOS of 450 nM, 30 uM, and >500 uM, respectively; inhibits cellular nitrate/nitrite synthesis in RAW, rat mesangium, and human embryonic kidney 293 cells with IC50 values 40- to 100-fold higher than at the isolated enzyme; dose-dependently suppresses the LPS-induced increase in plasma nitrate/nitrite (NO(x)) levels with ED50 of 14.9 micromol/kg/h, partially restores normal blood pressure responses to norepinephrine and sodium nitroprusside in model of LPS-induced vascular hyporesponsiveness.

GY06555

GW274150

210354-22-6

GW274150 is a potent and highly selective inhibitor of iNOS with IC50 of 1.4 uM, displays >200 fold selectivity over eNOS and nNOS (IC50>100 uM); attenuates the degree of chronic inflammation and tissue damage associated with collagen-induced arthritis in mice; significantly reduces serum urea, serum creatinine, AST, and NAG, reduces experimental renal ischemia/reperfusion injury.

GY03332

L-NAME hydrochloride

51298-62-5

L-NAME hydrochloride is a widely used inhibitor of NO synthase (NOS) with IC50 of 70 uM for purified brain NOS; inhibits cGMP formation in endothelial cells with an IC50 of 3.1 µM (in the presence of 30 µM arginine) and reverses the vasodilation effects of acetylcholine in rat aorta rings.

GY06514

ATV399

393834-37-2

ATV399 (ATV-399) is a novel small molecule that dose-dependently reduces the cleaved caspase9 levels with IC50 of 3.3 uM, inhibits dimerization of iNOS; inhibits cleaved caspase-9 activation and subsequent β-cell apoptosis induced by a combination of IL-1β, IFN-γ and high glucose.

GY06493

BYK191023

608880-48-4

BYK191023 (BYK-191023) is a potent, highly selective inhibitor of inducible nitric-oxide synthase (iNOS) with IC50 of 86 nM, >20-fold selectivity over nNOS and eNOS (IC50=17 and 162 uM); exhibits an affinity for iNOS, nNOS, and eNOS of 450 nM, 30 uM, and >500 uM, respectively; inhibits cellular nitrate/nitrite synthesis in RAW, rat mesangium, and human embryonic kidney 293 cells with IC50 values 40- to 100-fold higher than at the isolated enzyme; dose-dependently suppresses the LPS-induced increase in plasma nitrate/nitrite (NO(x)) levels with ED50 of 14.9 micromol/kg/h, partially restores normal blood pressure responses to norepinephrine and sodium nitroprusside in model of LPS-induced vascular hyporesponsiveness.

GY06483

3-Bromo-7-Nitroindazole

74209-34-0

3-Bromo-7-Nitroindazole is a more potent inhibitor of nNOS than 7-nitroindazole in vitro, is also potent against iNOS, inhibits rat nNOS, bovine eNOS, and rat iNOS with IC50 of 0.17, 0.86, and 0.29 uM.

GY05655

CAT639

CAT639(CAT 639;CAT-639) is an improved analog of ATV399 that exhibits improved β-cell viability and insulin secretion in the rat insulin-producing INS1E cells and primary rat dispersed islet cells, inhibits dimerization of iNOS; reduces the production of nitric oxide (NO) by allosterically inhibiting dimerization of the inducible nitric oxide synthase (iNOS) without affecting its mRNA levels; robustly inhibitscaspase-9 activity at sub-micromolar levels (IC50=0.48 uM), also exhibits potent inhibition of CYP3A4; protects primary rat islet survival and function impaired by cytokines.

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