n-terminally acetylated endomorphin-1

N-terminally acetylated Endomorphin-1 is a modified Endomorphin-1.

N-terminally acetylated Endomorphin-1 acetate (Ac-L-Tyr-L-Pro-L-Trp-L-Phe-CONH2) is a modified Endomorphin-1.

Leu-enkephalin, an endogenous peptide consisting of five amino acids, functions as an agonist at opioid receptors. The N-terminally acetylated form of this compound is known as N-terminally acetylated Leu-enkephalin.

N-terminally acetylated Leu-enkephalin is the N-terminally acetylated form of Leu-enkephalin.

E-2078, known chemically as (N-Me-Tyr1,N-Me-Arg7,D-Leu-NHEt8)-Dynorphin A (1-8), is a stable analog of Dynorphin A (1–8) and functions as a kappa opioid receptor (KOR) agonist [1].

(S)-N-(1-Amino-5-guanidino-1-oxopentan-2-yl)benzamide hydrochloride is a useful organic compound for research related to life sciences. The catalog number is T65350 and the CAS number is 4299-03-0.

Endomorphin 1 is a high affinity and selective agonist of the μ-opioid receptor and displays reasonable affinities for kappa3 binding sites (Ki: 20~30 nM).

Inhibits neural Wiskott-Aldrich syndrome protein (N-WASP) by stabilizing the autoinhibited state of the protein. Blocks phosphatidylinositol 4,5-bisphosphate (PIP2)-stimulated actin assembly (IC50 ~ 2 μM) but does not directly inhibit actin polymerization

Endomorphin-1 acetate is a highly selective and high-affinity μ-opioid receptor agonist (K i: 1.11 nM) that also demonstrates moderate affinity for kappa 3 binding sites (K i: 20-30 nM). This compound exhibits antinociceptive properties.

187-1, N-WASP Inhibitor TFA, a 14-amino acid cyclic peptide, serves as an allosteric inhibitor of the neural Wiskott-Aldrich syndrome protein (N-WASP). This compound effectively suppresses actin assembly triggered by phosphatidylinositol 4,5-bisphosphate (PIP2), exhibiting a potent inhibitory concentration (IC 50) of 2 μM. Furthermore, 187-1, N-WASP Inhibitor TFA inhibits the activation of the Arp2/3 complex by N-WASP, maintaining the protein in its autoinhibited state, ensuring the prevention of its activation.