167114-91-2

Basic information

• Product Name: AUTOCAMTIDE-2-RELATED INHIBITORY PEPTIDE
• Synonyms: (ALA9)-AUTOCAMTIDE-2;ALS9 AUTOCAMTIDE 2;ALP;LYS-LYS-ALA-LEU-ARG-ARG-GLN-GLU-ALA-VAL-ASP-ALA-LEU;KKALRRQEAVDAL;AUTOCAMTIDE 2-RELATED INHIBITORY PEPTIDE, MYRISTOYLATED TRIFLUOROACETATE SALT;AUTOCAMTIDE-2-RELATED INHIBITORY PEPTIDE;ESKINE
• CAS NO: 167114-91-2
• Molecular Formula: C80H143F3N22O22
• Molecular Weight: 1822.12
• Product Categories: Intracellular receptor
• Mol File: 167114-91-2.mol
• Article Data: 0

Chemical Properties

• Appearance: white/lyophilized powder
• Storage Temp.: −20°C
• Solubility: H2O: soluble
• CAS DataBase Reference: AUTOCAMTIDE-2-RELATED INHIBITORY PEPTIDE(CAS DataBase Reference)
• NIST Chemistry Reference: AUTOCAMTIDE-2-RELATED INHIBITORY PEPTIDE(167114-91-2)
• EPA Substance Registry System: AUTOCAMTIDE-2-RELATED INHIBITORY PEPTIDE(167114-91-2)

Safety Data

• Hazard Codes: Xn,F
• Statements: 20/21/22-36-11
• Safety Statements: 22-24/25-26-36/37-16
• WGK Germany: 3
• Hazardous Substances Data: 167114-91-2(Hazardous Substances Data)

Usage

Description

AUTOCAMTIDE-2-RELATED INHIBITORY PEPTIDE is a small peptide derived from autocamte, a protein found in the brain. It is known for its high specificity and potency in inhibiting calmodulin kinase II (CaMKII), a key enzyme involved in various cellular processes. This peptide has garnered significant interest due to its potential applications in understanding and treating various diseases and conditions.

Uses

Used in Pharmaceutical Research:
AUTOCAMTIDE-2-RELATED INHIBITORY PEPTIDE is used as a research tool for studying the role of CaMKII in various cellular processes and diseases. Its high specificity and potency make it an ideal candidate for investigating the molecular mechanisms underlying CaMKII-mediated signaling pathways.
Used in Theileria Infections:
In the context of virulent Theileria infections, AUTOCAMTIDE-2-RELATED INHIBITORY PEPTIDE is used as an inhibitor to target CaMKII action in infected macrophages. This application aims to better understand the role of CaMKII in the pathogenesis of Theileria infections and potentially develop novel therapeutic strategies.
Used in Neural Cell Death Research:
AUTOCAMTIDE-2-RELATED INHIBITORY PEPTIDE is employed in neonatal hippocampal slice cultures to study its influence on oxidative stress associated with neural cell death after hypoxia-ischemia. This application seeks to elucidate the role of CaMKII in neurodegenerative processes and identify potential targets for neuroprotective interventions.
Used in GTPase-Activating Protein Studies:
AUTOCAMTIDE-2-RELATED INHIBITORY PEPTIDE is used as a quenching agent to study the phosphorylation of recombinant synGA (GTPase-activating protein) induced by CaMKII. This application helps researchers understand the interplay between CaMKII and GTPase-activating proteins, which may have implications for the development of new therapeutic approaches for various diseases.

Biological Activity

synthetic peptide aip (autocamtide-2-related inhibitory peptide) is a nonphosphorylatable analog of autocamtide-2, which was identified to be a highly specific and potent inhibitor of calmodulin-dependent protein kinase ii (cam-kinase ii, camkii). camkii is a serine/threonine-specific protein kinase, which is modulated by the ca2+/calmodulin.

Biochem/physiol Actions

Calmodulin kinase II facilitates the calcium-dependent L-type calcium channels. Autocamtide 2-related inhibitory peptide action does not influence cAMP (cyclic adenosine monophosphate)-dependent protein kinase II, calmodulin-dependent protein kinase IV and protein kinase C. Increased expression of calmodulin kinase II is observed in structural heart disease, indicated by myocardial infarction. Thus, inhibition of calmodulin kinase II activity might serve as a protective effect against structural heart disease, as it is found to prevent cardiac hypertrophy, dilation and dysfunction.

in vitro

aip (1 mm) completely inhibited camkii activity, but did not affect camp-dependent protein kinase, calmodulin-dependent protein kinase iv and protein kinase c,. the inhibition was noncompetitive, and the action was caused by binding to the autophosphorylation site, which is distinc from that for the exogenous substrate. the ic50 for the autophosphorylation of cam ii is 100 nm [1].

in vivo

mice treated with aip by transgenic expression of aip, were protected from fructose-rich diet-induced arrhythmogenesis, spontaneous contractions and spontaneous ca2+ release events [2]. intra-nucleus accumbens (nac) injection of aip could dose-dependently increase the hwl (hindpaw withdrawal latency) to noxious thermal and mechanical stimulation in rats with mononeuropathy [3].

IC 50

40 nm for cam-kinase ii [1].

references

[1] ishida a1, kameshita i, okuno s, kitani t, fujisawa h. a novel highly specific and potent inhibitor of calmodulin-dependent protein kinase ii. biochem biophys res commun. 1995 jul 26;212(3):806-12.[2] sommese l, valverde ca, blanco p, castro mc, rueda ov, kaetzel m, dedman j, anderson me, mattiazzi a, palomeque j. ryanodine receptor phosphorylation by camkii promotes spontaneous ca(2+) release events in a rodent model of early stage diabetes: the arrhythmogenic substrate. int j cardiol. 2016 jan 1;202:394-406.[3] bian h, yu lc. intra-nucleus accumbens administration of the calcium/calmodulin-dependent protein kinase ii inhibitor aip induced antinociception in rats with mononeuropathy. neurosci lett. 2015 jul 10;599:129-32.