L-Arginine is the nitrogen donor for synthesis of nitric oxide, a potent vasodilator that is deficient during times of sickle cell crisis.Target: OthersL-Arginine is an α-amino acid. It was first isolated in 1886. The L-form is one of the 20 most common natural amino acids. At the level of molecular genetics, in the structure of the messenger ribonucleic acid mRNA, CGU, CGC, CGA, CGG, AGA, and AGG, are the triplets of nucleotide bases or codons that code for arginine during protein synthesis. In mammals, arginine is classified as a semiessential or conditionally essential amino acid, depending on the developmental stage and health status of the individual.L-Arginine is associated with a decrease in cardiac index while stroke index is maintained in patients with severe sepsis. Resolution of shock at 72 hours is achieved by 40% and 24% of the patients in the L-Arginine and placebo cohorts, respectively. L-Arginine (450 mg/kg during a 15-minute period) amplifies and sustains the hyperemia (38%) and increases absolute brain blood flow after eNOS upregulation by chronic simvastatin treatment (2 mg/kg subcutaneously, daily for 14 days) in SV-129 mice.
Kuwanon A is a flavone derivative isolated from the root barks of the mulberry tree (Morus alba L.); inhibits nitric oxide production with an IC50 of 10.5 μM.
Methylene blue trihydrate (C.I. Basic Blue 9 trihydrate) is a guanylyl cyclase (sGC), monoamine oxidase A (MAO-A) and NO synthase (NOS) inhibitor. Methylene blue trihydrate is a vasopressor and is often used as a dye in several medical procedures. Methylene blue trihydrate has antinociception, antimalarial, antidepressant and anxiolytic activity effects. Methylene Blue trihydrate has the potential for methemoglobinemias, neurodegenerative disorders and ifosfamide-induced encephalopathytreatment[1][2][3].
6-Methoxynaringenin is a natural flavonoid that inhibits NO production with an IC50 of 25.8 μM[1].
L-Arginine-13C6,15N4 ((S)-(+)-Arginine-13C6,15N4) hydrochloride is the 13C- and 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.
Prim-O-glucosylcimifugin exerts anti-inflammatory effects through the inhibition of iNOS and COX-2 expression by through regulating JAK2/STAT3 signaling.
NOS-IN-3 (Compound 9a) is a potent, selective, imidamide derived NOS inhibitor with an IC50 against iNOS of 4.6 µM, without inhibiting eNOS. NOS-IN-3 has little toxicity and can be studied in the treatment of inducible isoform involved diseases, such as septic shock[1].
Coenzyme Q0 (CoQ0) is a potent, oral active ubiquinone compound can be derived from Antrodia cinnamomea. Coenzyme Q0 induces apoptosis and autophagy, suppresses of HER-2/AKT/mTOR signaling to potentiate the apoptosis and autophagy mechanisms. Coenzyme Q0 regulates NFκB/AP-1 activation and enhances Nrf2 stabilization in attenuation of inflammation and redox imbalance. Coenzyme Q0 has anti-angiogenic activity through downregulation of MMP-9/NF-κB and upregulation of HO-1 signaling[1][2][3].
Methylene blue (Basic Blue 9) hydrate is a guanylyl cyclase (sGC), monoamine oxidase A (MAO-A) and NO synthase (NOS) inhibitor. Methylene blue is a vasopressor and is often used as a dye in several medical procedures. Methylene blue hydrate through the nitric oxide syntase/guanylate cyclase signalling pathway to reduce prepulse inhibition. Methylene blue hydrate is a REDOX cycling compound and able to cross the blood-brain barrier. Methylene blue hydrate is a Tau aggregation inhibitor. Methylene blue hydrate reduces cerebral edema, attenuated microglial activation and reduced neuroinflammation[1][2][3].
Mifepristone is a progesterone receptor (PR) and glucocorticoid receptor (GR) antagonist with IC50s of 0.2 nM and 2.6 nM in in vitro assay.
Amaroswerin is a bioactive secoiridoid glucoside from Swertia mussotii. Amaroswerin has anti-inflammatory, antidiabetic, antiviral, anticholinergic and immunomodulatory activities. Amaroswerin inhibits NO release with an IC50 value of 5.42 μg/mL in RAW264.7 cells[1].
L-NAME hydrochloride inhibits NOS with an IC50 of 70 μM. L-NAME is a precursor to NOS inhibitor L-NOARG which has an IC50 value of 1.4 μM.
Regaloside A, a phenylpropanoid, shows significant DPPH radical scavenging activity of 58.0% at 160 ppm. Regaloside A has anti-inflammatory activity[1].
Regaloside B is a phenylpropanoid isolated from Lilium longiflorum. Regaloside B can inhibit the expression of iNOS and COX-2, has anti-inflammatory activity[1][2].
O-Acetylschisantherin L (Acetylschisantherin L) is a natural lignan, which exhibits inhibitory effects on LPS-induced NO production in BV-2 cells with an IC50 of 23.1 μM[1].
Valeriandoid F is an iridoid, which potently inhibits NO production with an IC50 value of 0.88 μM. Valeriandoid F has anti-inflammatory and antiproliferative activities[1].
Camstatin, a functionally active 25-residue fragment of PEP-19's IQ motif, binds calmodulin and inhibits neuronal nitric oxide (NO) synthase[1].
COX-2-IN-32 (Compound 2f) is an iNOS and COX-2 inhibitor. COX-2-IN-32 decreases the expression of NF-κB. COX-2-IN-32 has anti-inflammatory activity by inhibits NO production in LPS-induced RAW264.7 macrophages (IC50: 11.2 μM)[1].
L-Arginine-1,2-13C2 ((S)-(+)-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.
NF-κB/MAPK-IN-1 (compound 11a) is a potent inhibitor of NF-κB and MAPK pathway. NF-κB/MAPK-IN-1 shows inhibitory activity against NO production, with an IC50 of 6.96 µM. NF-κB/MAPK-IN-1 suppresses LPS-induced iNOS, COX-2, ERΚ and P38 signaling activation. NF-κB/MAPK-IN-1 can prevent LPS induced inflammatory response in macrophages. NF-κB/MAPK-IN-1 can be used for rheumatoid arthritis (RA) research[1].
Pectolinarin, isolated from Cirsium chanroenicum, possesses anti-inflammatory activity[1]. Pectolinarin inhibits secretion of IL-6 and IL-8, as well as the production of PGE2 and NO. Pectolinarin suppresses cell proliferation and inflammatory response and induces apoptosis via inactivation of the PI3K/Akt pathway[2].
3-Bromo-7-nitroindazole is a more potent and selective inhibitor of neuronal nitric oxide synthase (nNOS) than eNOS or inducible nitric oxide synthase (iNOS). 3-Bromo-7-nitroindazole affects the intercellular messenger nitric oxide (NO) synthesis throughout the body and brain[1].
PPM-18 (NSC 73233), a potent anti-inflammatory agent, inhibits nitric oxide synthase expression. PPM-18 is a potent inhibitor of iNOS expression by blocking the binding of NF-κB to promoter[1]. PPM-18, an analog of Vitamin K, induces autophagy and apoptosis in bladder cancer cells through ROS and AMPK signaling pathways[2].
L-Arginine is the nitrogen donor for synthesis of nitric oxide, a potent vasodilator that is deficient during times of sickle cell crisis.Target: OthersArginine is an α-amino acid. It was first isolated in 1886. The L-form is one of the 20 most common natural amino acids. At the level of molecular genetics, in the structure of the messenger ribonucleic acid mRNA, CGU, CGC, CGA, CGG, AGA, and AGG, are the triplets of nucleotide bases or codons that code for arginine during protein synthesis. In mammals, arginine is classified as a semiessential or conditionally essential amino acid, depending on the developmental stage and health status of the individual.L-Arginine is associated with a decrease in cardiac index while stroke index is maintained in patients with severe sepsis. Resolution of shock at 72 hours is achieved by 40% and 24% of the patients in the L-Arginine and placebo cohorts, respectively. L-Arginine (450 mg/kg during a 15-minute period) amplifies and sustains the hyperemia (38%) and increases absolute brain blood flow after eNOS upregulation by chronic simvastatin treatment (2 mg/kg subcutaneously, daily for 14 days) in SV-129 mice.
Agmatine sulfate exerts modulatory action at multiple molecular targets, such as neurotransmitter systems, ion channels and nitric oxide synthesis. It is an endogenous agonist at imidazoline receptor and a NO synthase inhibitor.
3-O-Acetyl-16α-hydroxydehydrotrametenolic acid, an anti-inflammatory triterpenoid, inhibits NO production and iNOS expression in LPS-stimulated Raw264.7 cells[1].
Avanafil (TA-1790) dibenzenesulfonate is a potent and selective phosphodiesterase-5 (PDE-5) inhibitor with IC50 values of 5.2 nM, 630 nM, 5700 nM, 6200 nM, 12000 nM, 27000 nM, 51000 nM and 53000 nM for PDE-5, PDE-6, PDE-4, PDE-10, PDE-8, PDE-7, PDE-2 and PDE-1, respectively. Avanafil dibenzenesulfonate activates NO/cGMP/PKG signaling-pathway to decrease loss in BMD, bone atrophy, and oxidative stress. Avanafil dibenzenesulfonate inhibits cyclic guanosine monophosphate (cGMP) hydrolysis and thus increases cGMP levels. Avanafil dibenzenesulfonate can be used for the research of erectile dysfunction and osteoporosis[1][2][3].
Isophysalin A is a physalin with alpha and beta unsaturated ketone components. Isophysalin A binds to GSH and targets multiple cysteine residues on IKKβ. Isophysalin A also inhibits inducible NO synthase (iNOS) and nitric oxide (NO) production, showing anti-inflammatory activity[1].
Carboxy-PTIO is a potent nitric oxide (NO) scavenger that can make a quick reaction with NO to produce NO2. Carboxy-PTIO can prevent hypotension and endotoxic shock through the direct scavenging action against NO in lipopolysaccharide-stimulated rat model[1][2][3].
Flazin is a non-enzymatic protein glycation inhibitor, also inhibits peroxynitrite (ONOO-), with an IC50 value of 85.31 μM for bovine serum albumin (BSA) glycation and an EC50 value of 71.99 μM for ONOO-. Flazin can be used for researching diabetes and neuronal disorders. Flazin also can used as a lipid droplet (LD) regulator against lipid disorders, and a xanthine oxidase (XOD) inhibitor[1][2][3].