pkc α

PKC β pseudosubstrate acetate (PKC β pseudosubstrate acetate (172308-76-8 Free base)) is a selective cell-permeable inhibitor of PKC.

PKC β pseudosubstrate TFA is a selective, cell-permeable inhibitor of PKC [1].

PKCδ Peptide Substrate is a highly specific substrate for the δ-type of Protein kinase C, composed of a sequence that mirrors murine eEF-1α (422-443) and includes Thr-431 [1].

PKCβII Peptide Inhibitor I, a specific PKCβII inhibitor, exhibits cardioprotective properties in a rat cardiac ischemia/reperfusion injury model and mitigates vascular endothelial dysfunction [1].

PKCε (85-92) (ψεRACK) is a peptide and selective PKCε activator that does not affect the activity of other PKC isozymes.PKCε (85-92) induces a pro-angiogenic response in endothelial cells, promotes FGF-2 cytosolization, and regulates VEGF activity.

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].

PKCα (C2-4) inhibitor peptide is a specific antagonist to PKCα, preventing the α1A-adrenoreceptor agonist A-61603 [1] from inhibiting I_Kr.

Myristoylated PKCθ pseudosubstrate peptide inhibitor is a synthetic peptide utilized to investigate the mechanism of action of protein kinase C theta (PKCθ) [1].

Myristoylated PKCη pseudosubstrate inhibitor is a cell-permeable compound utilized to investigate the mechanism of action of PKCη [1].

Myristoylated protein kinase C inhibitor 20-28 (PKC 20-28,myristoylated) is a cell-permeable inhibitor of protein kinase C, utilized in cancer research [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].

PKC-ε Translocation Inhibitor Peptide is a selective modulator that controls the FcγR-mediated internalization rate of opsonized beads without affecting FcαR trafficking [1].

Selective cell-permeable peptide inhibitor of protein kinase C (IC50 ~ 0.5 μM). Consists of amino acids 19 - 31 of PKC pseudosubstrate domain linked by a disulphide bridge to a cell permeabilisation Antennapedia domain vector peptide. The Antennapedia pep

Delcasertib acetate is a selective δ protein kinase C (δPKC) inhibitor for the study of acute myocardial infarction and pain.

Protein Kinase C (alpha) Peptide (TFA) is a PKC-α-associated peptide functioning as a lipid-dependent serine/threonine protein kinase. It plays a pivotal role in regulating several cellular functions such as survival, proliferation, differentiation, migration, and adhesion [1].

Delcasertib (KAI-9803) is a potent and selective inhibitor of δ-protein kinase C (δPKC).

Epsilon-V1-2 has been extensively investigated for its function as a PKC epsilon (PKCε) inhibitor. Epsilon-V1-2 has been widely applied in studies addressing ovarian aging, apoptosis in human granulosa cells, cerebral ischemia-reperfusion injury, brain development, hepatocyte insulin signaling, and neuronal cell death under ischemic conditions. Epsilon-V1-2 has been shown to effectively reduce PKCε activity, thereby enabling detailed exploration of regulatory pathways involving mitochondrial dynamics, calcium overload, AKT activation, brain atrophy, insulin resistance, and ferroptosis. Epsilon-V1-2 demonstrates notable therapeutic relevance in models of stroke, SHORT syndrome, hepatic steatosis, and brain injury, supporting its continued evaluation as a potential pharmacological agent across multiple disease contexts.

Delcasertib (KAI-9803) hydrochloride, a potent and selective δ-protein kinase C (δPKC) inhibitor, shows promise in reducing ischemia and reperfusion injury in animal models of acute myocardial infarction (MI) [1] [2].

Myristoylated TFA Pep2m (Myr-Pep2m TFA) is a cell-permeable peptide that effectively disrupts the interactions between the protein kinase ζ (PKMζ) downstream targets—N-ethylmaleimide-sensitive factor/glutamate receptor subunit 2 (NSF/GluR2). PKMζ, an autonomously active isozyme of protein kinase C (PKC), plays a crucial role in these interactions [1] [2].

Malantide TFA, a synthetic dodecapeptide, originates from the phosphorylation site targeted by cAMP-dependent protein kinase (PKA) on the β-subunit of phosphorylase kinase. Exhibiting a high specificity for PKA with a Michaelis constant (Km) of 15 μM, this compound demonstrates more than 90% inhibition of substrate phosphorylation in the presence of protein inhibitor (PKI) across various rat tissue extracts [1]. Moreover, Malantide TFA acts as an effective substrate for Protein Kinase C (PKC) with a Km of 16 μM [2].

Protein Kinase C (19-31) TFA is a peptide inhibitor derived from the pseudo-substrate regulatory domain of PKCa (residues 19-31), featuring a serine substitution for alanine at position 25. It serves as a substrate peptide for evaluating Protein Kinase C (PKC) activity, playing a crucial role in modulating protein functions by phosphorylating the hydroxyl groups of serine and threonine amino acids on target proteins [1] [2].

Myelin Basic Protein (MHP4-14) TFA, a synthetic peptide comprising residues 4-14 of myelin basic protein, serves as a highly selective substrate for protein kinase C (PKC) with a K_m of 7 μM. It is not phosphorylated by cyclic AMP-dependent protein kinase, casein kinases I and II, Ca^2+/calmodulin-dependent protein kinase II, or phosphorylase kinase, making it an ideal candidate for protein kinase C assays in crude tissue extracts, ensuring minimal background interference [1] [2].

N-Myristoyl-Lys-Arg-Thr-Leu-Arg is a protein kinase C (PKC) inhibitor (IC50 = 75 μM) that effectively inhibits IL-2 receptor induction and IL-2 production in the human leukemic cell line Jurkat [1].

RNAENFDRF (βIIPKC624-632) conjugated to TAT47-57, a cell-permeable peptide, forms SAMβA, a rationally designed peptide that selectively antagonizes Mfn1-βIIPKC association. SAMβA acts as a selective inhibitor of mitofusin 1-βIIPKC association, demonstrating improved heart failure outcomes in rats [1].