NO Synthase Activator

Dipeptide 2 (N-Valyltryptophan) is an orally active, competitive angiotensin-converting enzyme (ACE) inhibitory peptide with an IC₅₀ of 10.50 μM. Dipeptide 2 reduces intracellular Calcium ions. Dipeptide 2 significantly increases the content of NO, inhibits the production of ET-1, and induces the phosphorylation of eNOS. Dipeptide 2 decreases the systolic and diastolic blood pressure of spontaneously hypertensive rats.

Demethylasterriquinone B1 (DAQ B1; L-783281) is an orally active insulin receptor (insulin receptor) agonist and AKT activator. By activating AKT, Demethylasterriquinone B1 upregulates the expression and activity of eNOS to increase NO production, while downregulating the expression of the NADPH oxidase subunit p22phox to reduce oxidative stress and improve vascular endothelial dysfunction in hypertensive rats. Demethylasterriquinone B1 combind with an AKT inhibitor targets the insulin signaling pathway to activate two antiviral pathways, RNA interference and JAK/STAT, in mosquitoes, thereby reducing Zika virus infection.

Gomisin J is a Schisandra chinensis-derived lignan that can inhibit multiple targets such as eNOS, AMPK (LKB1, CaMKIIβ), fetuin-A, NF-κB, Nrf2/HO-1, and can pass through the blood-brain barrier. Gomisin J increases NO bioavailability by activating eNOS, regulates lipid metabolism by activating the AMPK pathway, inhibits fetuin-A and NF-κB to exert anti-inflammatory effects, and activates Nrf2/HO-1 to enhance antioxidant capacity. Gomisin J has the activities of anti-hypertension, regulating liver lipid metabolism, and reducing cerebral ischemia-reperfusion injury, and can be used for research on hypertension, non-alcoholic fatty liver disease, cerebral ischemia-reperfusion injury, etc.

High density lipoprotein (human) (HDL (human)) is a human-derived high-density lipoprotein. High density lipoprotein can cross the blood-brain barrier, and partially acts on endothelial nitric oxide synthase (eNOS) by activating surface receptors such as SR-B1 and S1P3R, as well as intracellular signaling cascades involving Akt, PI3K and MAPK, thereby inducing the production of NO in endothelial cells. High density lipoprotein (human) can be used in research related to type 2 diabetes, Alzheimer's disease, cancer and atherosclerosis.

L-Arginine-¹⁵N₂ (hydrochloride) is the ¹⁵N-labeled L-Arginine (hydrochloride). L-Arginine hydrochloride ((S)-(+)-Arginine hydrochloride) is the nitrogen donor for synthesis of nitric oxide, a potent vasodilator that is deficient during times of sickle cell crisis.

3',4'-Dihydroxyflavonol (DiOHF) is an effective antioxidant, which reduces superoxide and improves nitric oxide (NO) function in diabetic rat mesenteric arteries.

AVE3085 is a potent endothelial nitric oxide synthase enhancer, used for cardiovascular disease treatment.

Quinocetone is an orally active animal feed additive used to increase the meat production of livestock and poultry. Quinocetone exhibits antibacterial activity against a variety of pathogenic microorganisms. Quinocetone exhibits tissue-specific (liver, lymphocyte) toxicity. Quinocetone induces autophagy in cells through the ATF6/DAPK1 pathway. Quinocetone activates the NF-κB and iNOS pathways, leading to cell apoptosis, hepatocyte vacuolar degeneration and fibrosis. Quinocetone can inhibit Nrf2/HO-1 and induce the generation of reactive oxygen species (ROS), leading to oxidative stress and DNA damage.

9 (10)-Nitrooleate (9(10)-Nitrated oleic acid) is an endogenous lipid signaling mediator with vasoprotective effects. 9 (10)-Nitrooleate enhances enzymatic activity and improves nitric oxide bioavailability by inducing phosphorylation of Akt and ERK1/2, regulating the multi-site phosphorylation status of eNOS and optimizing its interaction with Hsp90. 9 (10)-Nitrooleate also activates PPARα, PPARδ and PPARγ receptors, thereby regulating adipogenesis, glucose uptake and inflammation-related gene expression, and exhibits immunosuppressive effects by inhibiting neutrophil migration and cytokine secretion. 9 (10)-Nitrooleate is widely used in studies of sepsis and related inflammatory diseases.

JS-K is a NO donor that reacts with glutathione to generate NO at physiological pH. JS-K induces reactive oxygen species (ROS) to mediate apoptosis. JS-K induces autophagy. JS-K inhibits invasion. JS-K has a broad spectrum anti-proliferative activity in cancer cells. JS-K reduces tumor volume and causes necrosis of implanted tumors in mice.

L-Arginine-1,2-¹³C₂ (hydrochloride) is the ¹³C-labeled L-Arginine hydrochloride. L-Arginine hydrochloride ((S)-(+)-Arginine hydrochloride) is the nitrogen donor for synthesis of nitric oxide, a potent vasodilator that is deficient during times of sickle cell crisis.

TP508 TFA is a 23-amino acid nonproteolytic thrombin peptide that represents a portion of the receptor-binding domain of thrombin molecule. TP508 TFA activates endothelial NO synthase (eNOS) and stimulates production of NO in human endothelial cells. TP508 TFA activates endothelial cells and stem cells to revascularize and regenerate tissues.

Bendazol is an orally effective antihypertensive agent. Bendazol acts directly on vascular smooth muscle to dilate blood vessels and reduce peripheral resistance, thereby improving blood circulation. Bendazol significantly inhibits the development of myopia in rabbit models. Bendazol can regulate kidney function by increasing the activity of NO synthase in the rat model of nephrogenic hypertension. In addition, Bendazol has an effect on sexual behavior and spermatogenesis in male rats.

L-Arginine-1-¹³C (hydrochloride) is the ¹³C-labeled L-Arginine hydrochloride. L-Arginine hydrochloride ((S)-(+)-Arginine hydrochloride) is the nitrogen donor for synthesis of nitric oxide, a potent vasodilator that is deficient during times of sickle cell crisis.

Quinolinic acid-13C4, 15N is an isotopic labeled Quinolinic acid (HY-100807). Quinolinic acid, an endogenous metabolite of tryptophan, is a N-methyl-D-aspartate receptor (NMDA receptor) agonist. Quinolinic acid increases glutamate efflux, induces the generation of ROS, activates nitric oxide synthase, produces excessive NO, leading to calcium ion influx and neuronal apoptosis.

Benzanthrone is an immunotoxic, pro-inflammatory Photosensitizer. Benzanthrone upregulates iNOS, COX-2 and inflammatory cytokines; activates ERK1/2, p38, JNK, AP-1 and NF-κB; inhibits Nrf2; and induces oxidative stress and DNA damage. Upon radiation exposure, Benzanthrone generates singlet oxygen and superoxide anion radicals, induces photohemolysis and lipid peroxidation, and alters the levels of skin xenobiotic enzymes. Benzanthrone exhibits differential genotoxicity in different cell lines. Benzanthrone possesses skin tumor-initiating and promoting activities. Benzanthrone can be used in skin tumor-related studies.

Zofenoprilat is an angiotensin-converting enzyme (ACE) inhibitor with an IC₅₀ of 1.7 nM. Zofenoprilat exerts cardioprotective and renoprotective effects by inhibiting angiotensin II expression and lowering blood pressure. Zofenoprilat promotes NO production and reduces endothelin-1 (ET-1) expression. Zofenoprilat decreases TNFα-induced ROS production and protects vascular endothelial function. Zofenoprilat regulates oxidative stress-related molecules and possesses antioxidant activity. Zofenoprilat can be used in studies related to hypertension and congestive heart failure.

Banoxantrone (AQ4N), as a prototype hypoxia selective cytotoxin, can be reduced to AQ4, a potent topoisomerase II inhibitor. Banoxantrone selectively kills hypoxic cells via an iNOS-dependent mechanism. Banoxantrone shows a potent cytotoxicity and hypoxia-selective effect enhanced by radiation.

AVE-9488 is an eNOS enhancer with the activity of protecting the heart from ischemia-reperfusion injury. AVE-9488 can upregulate eNOS expression, increase NO production, reduce myocardial ischemia-reperfusion injury, and reduce the level of reactive oxygen species.

L-Arginine (hydrochloride) (Standard) is the analytical standard of L-Arginine (hydrochloride). This product is intended for research and analytical applications. L-Arginine ((S)-(+)-Arginine) is the substrate for the endothelial nitric oxide synthase (eNOS) to generate NO. L-Arginine is transported into vascular smooth muscle cells by the cationic amino acid transporter family of proteins where it is metabolized to nitric oxide (NO), polyamines, or L-proline. L-Arginine is a potent vasodilator, and can be used to induce experimental acute pancreatitis.