nitric

Nitric Oxide Synthase (599-613) Blocking Peptide, Bovine Endothelial Cell (Ac-Pro-Tyr-Asn-Ser-Ser-Pro-Arg-Pro-Glu-Gln-His-Lys-Ser-Tyr-Lys-Cys) is a peptide that inhibits the function of NOSs as a result it blocks the production of NO. Because of the invol

Bradykinin is an inflammatory mediator. It is a peptide that causes blood vessels to dilate (enlarge) via the release of prostacyclin, nitric oxide, and Endothelium-Derived Hyperpolarizing Factor. Bradykinin is a physiologically and pharmacologically active peptide of the kinin group of proteins, consisting of nine amino acids.

N'-Nitro-D-arginine (N'-Nitro-D-arginine) is a Building Block.

Camstatin acetate binds calmodulin and inhibits neuronal nitric oxide synthase. Camstatin acetate is a functionally active 25-residue fragment of the single calmodulin-binding IQ motif of PEP-19.

Tat-NR2B9c acetate (NA-1 acetate) is a postsynaptic density-95 (PSD-95) inhibitor, with EC50 values of 6.7 nM and 670 nM for PSD-95d2 (PSD-95 PDZ domain 2) and PSD-95d1, respectively. Tat-NR2B9c acetate disrupts the PSD-95 NMDAR interaction, inhibiting NR2A and NR2B binding to PSD-95 with IC50 values of 0.5 μM and 8 μM, respectively. Tat-NR2B9c acetate also inhibits neuronal nitric oxide synthase (nNOS) PSD-95 interaction, and possesses neuroprotective efficacy.

L-hydroxy Arginine is a substrate for nitric oxide synthase in the catabolism of L-arginine to form nitric oxide. It has been used as a biomarker for reduced nitric oxide formation in patients with cardiovascular disease and metabolic syndrome.

PAR2 (1-6) is a synthetic peptide agonist of proteinase-activated receptor 2 (PAR2) that corresponds to residues 1-6 of the amino terminal tethered ligand sequence of mouse and rat PAR2. It also corresponds to residues 39-44 and 37-42 of the mouse and rat full-length sequences, respectively. PAR2 (1-6) induces relaxation in precontracted rat arteries in a concentration-dependent manner, an effect that can be reduced by the nitric oxide synthase inhibitor L-NNA . It inhibits keratinocyte growth in the presence and absence of growth factors. PAR2 (1-6) inhibits LPS-induced pulmonary neutrophil influx and increases in matrix metalloproteinase-2 (MMP-2) activity in mice.

Adrenomedullin (13-52) is a truncated form of adrenomedullin (1-52) . It induces nitric oxide-dependent relaxation of and inhibits release of angiotensin II and endothelin-1 from isolated rat aorta. In vivo, adrenomedullin (13-52) decreases mean arterial pressure (MAP) in spontaneously and renal hypertensive rats in a dose-dependent manner. Adrenomedullin (13-52) (10-3,000 ng per animal) reverses increases in lobar arterial pressure induced by U-46619 in a dose-dependent manner in cats but has no effect on basal lobar arterial pressure or systemic arterial pressure. It also potentiates inflammatory edema and neutrophil accumulation in rats.

Camstatin TFA, a 25-residue fragment derived from the IQ motif of PEP-19, effectively binds to calmodulin and inhibits neuronal nitric oxide (NO) synthase, demonstrating its functional activity [1].

Protein Kinase C (beta) Peptide, a fragment of Protein Kinase Cβ, is associated with hyperglycemia-induced decreases in endothelium-derived nitric oxide. Inhibiting Protein Kinase Cβ forestalls the impairment of endothelium-dependent vasodilation caused by acute hyperglycemia [1].

LL-37 GKE acetate, a peptide with 21 amino acids and the active structural domain of LL-37, inhibits lps-induced vascular nitric oxide production, is less toxic than LL-37 for hemolysis and apoptosis in human cultured smooth muscle cells, and possesses antimicrobial activity and therapeutic potential for sepsis.

FA-Ala-Arg is a dipeptide featuring a furylacryloyl group that degrades to yield arginine. It augments nitric oxide (NO) synthesis in MCF-7 cells through a mechanism in which cell-surface Carboxypeptidase-D (CPD) elevates intracellular arginine levels. Furthermore, FA-Ala-Arg promotes cell survival in prolactin (PRL)-treated cells wherein PRL modulates CPD mRNA levels [1].

PKC(85-92),Myristoylated is a myristic acid-conjugated, cell-permeable peptide activator of PKC that has been shown to increase nitric oxide (NO) release in cultured human umbilical vein endothelial cells (HUVECs) [1].

Myristoylated PKCε inhibitor peptide (Myr-PKCε-) is a cell-permeable inhibitor consisting of a peptide linked to myristic acid that specifically inhibits protein kinase C epsilon (PKCε), consequently diminishing nitric oxide (NO) release in cultured human umbilical vein endothelial cells (HUVECs) [1].

NCI 126224, a toll-like receptor 4 (TLR4) antagonist, demonstrates selective inhibition of nitric oxide (NO) production in RAW 264.7 macrophages, triggered by the TLR4 agonist LPS (IC50 = 0.31 µM), as opposed to minimal effects on NO production induced by agonists for TLR7/8 (R-848), TLR1/2 (Pam3CSK4), and TLR3 (poly(I:C)). Nevertheless, it also effectively inhibits NO production initiated by the TLR2/6 agonist FSL-1 at an IC50 of 0.6 µM in the same cell line. Moreover, NCI 126224 suppresses LPS-induced NF-κB activity in BV-2 microglial cells and reduces LPS-triggered increases in IL-1β and TNF-α levels in RAW 264.7 macrophages with IC50 values of 5.92, 0.42, and 1.54 µM, respectively.

Bradykinin (1-6) is an amino-truncated Bradykinin peptide and a stable metabolite of Bradykinin, cleaved by carboxypeptidase Y (CPY). This fragment of Bradykinin activates pain receptors and induces smooth muscle contraction.

Potent KV1.3 channel blocker (IC50 = 36 pM). Displays no effect at calcium-activated channels. Reduces VEGF-induced transmembrane calcium influxes and nitric oxide production in human endothelial cells.