inhibitory

IKKγ NBD Inhibitory Peptide acetate is a NEMO-binding domain peptide (NBD peptide) acetate corresponding to the NEMO amino-terminal alpha-helical region. IKKγ NBD Inhibitory Peptide acetate is shown to block TNF-alpha-induced NF-kB activation.

Autocamtide-2-related inhibitory peptide, myristoylated acetate is a CaM kinase II inhibitor; enhanced cell permeable derivative of Autocamtide-2-related inhibitory peptide.

Autocamtide-2-related inhibitory peptide is a potent and highly specific inhibitor of CaMKII, with an IC50 of 40 nM.

Dynamin inhibitory peptide Acetate is a peptide with the sequence Gln-Val-Pro-Ser-Arg-Pro-Asn-Arg-Ala-Pro that inhibit the GTPase dynamin.

Ras Inhibitory Peptide acetate is a peptide involved in the Ras-dependent signaling pathway that plays an important role in human cancers initiated by oncogenic receptors.

Autocamtide-2-related inhibitory peptide (TFA) is a highly specific and potent CaMKII inhibitor with an IC50 value of 40 nM.

Myristoylated Autocamtide-2-related inhibitory peptide, trifluoroacetic acid (TFA) form, is a potent and highly specific inhibitor of CaMKII, exhibiting an IC50 of 40 nM [1]. This compound constitutes the myristoylated variant of Autocamtide-2-related inhibitory peptide.

Dynamin Inhibitory Peptide TFA competitively inhibits the binding of dynamin to amphiphysin, effectively preventing endocytosis. Additionally, this compound impedes the dopamine D3's influence on GABA A receptors [1].

IKKγ NBD Inhibitory Peptide TFA is a specific NF-κB inhibitor that hinders the interaction between the IKKγ NEMO-binding domain (NBD) and IKKα and IKKβ, effectively preventing TNF-α-induced NF-κB activation. It has been demonstrated to significantly suppress inflammation and improve neurological deficits induced by cerebral ischemia [1] [2] [3].

[Tyr0] Gastric Inhibitory Peptide (23-42), human, is a glucose-dependent insulinotropic polypeptide (GIP) that modestly inhibits gastric acid secretion while enhancing insulin secretion, making it relevant for research on diabetes and obesity [1] [2].

Gastric Inhibitory Polypeptide (1-30), porcine, deficient in the 12 C-terminal amino acids of the natural gastric inhibitory polypeptide (GIP), demonstrates biological activity by enhancing the release of insulin and somatostatin [1].

Gastric Inhibitory Peptide (porcine), also known as a glucose-dependent insulinotropic polypeptide, is a 42-amino acid intestinal hormone that influences fat and glucose metabolism [1].

Acetyl Gastric Inhibitory Peptide (human), a fatty acid-derivatized analog of glucose-dependent insulinotropic polypeptide, exhibits enhanced antihyperglycemic and insulinotropic characteristics. This compound is utilized in diabetes, insulin resistance, and obesity research [1] [2] [3].

Acetyl Gastric Inhibitory Peptide (human) TFA, a fatty acid-derivatized analog of the glucose-dependent insulinotropic polypeptide, exhibits enhanced antihyperglycemic and insulinotropic properties. It is utilized in the research of diabetes, insulin resistance, and obesity [1] [2] [3].

TREM-1 inhibitory peptide M3 acts as a ligand-dependent antagonist of TREM-1, capable of suppressing systemic and pulmonary pro-inflammatory cytokine and chemokine production, thereby mitigating acute lung injury [1].

Gastric Inhibitory Polypeptide (6-30) amide (human) is an incretin hormone used in diabetes research [1].

Gastric inhibitory peptide (GIP) (1-42), an endogenous incretin hormone comprising 42 amino acids, promotes insulin secretion. Expressed in the intestinal neuroendocrine K cells and submandibular gland, it enters circulation after meals. GIP (1-42) blocks histamine, pentagastrin, and insulin-induced gastric acid and pepsin secretion, enhances glucose-stimulated insulin release, and accelerates gastric emptying in rats.

Gastric inhibitory peptide 1 (GIP-1) (3-42), a fragment of the incretin hormone GIP and antagonist to the GIP receptor, is generated through the action of serum dipeptidyl peptidase 4 (DDP-4). When administered at 25 nmol/kg to an ob/ob mouse diabetes model, GIP-1 (3-42) elevates plasma glucose levels and lowers plasma insulin levels, demonstrating its effect on reducing insulin secretion from BRIN-BD11 pancreatic cells at a concentration of 100 nM.

Gastric inhibitory peptide (GIP) (22-51), a pro-atherogenic peptide comprised of 30 amino acids from the residues 22-51 of its precursor protein proGIP, is present in human plasma. It activates the degradation of IκB-α and the nuclear translocation of NF-κB in both macrophage-differentiated THP-1 cells and human aortic endothelial cells at a concentration of 1 µM. Additionally, in ApoE-/- mice, GIP (22-51) escalates the area of atherosclerotic lesions and plaque development in vivo.

A cell-permeable synthetic peptide NEMO-binding domain peptide (NBD peptide) corresponding to the NEMO amino-terminal alpha-helical region is shown to block TNF-alpha-induced NF-kB activation. The interaction of IKγNEMO with the IKK complex is vital for t

Cell-permeable version of dynamin inhibitory peptide, an inhibitor of the GTPase dynamin that competitively blocks binding of dynamin to amphiphysin, preventing endocytosis. Reduces NMDA receptor internalization.

Dynamin inhibitory peptide, myristoylated acetate is a DynaMin inhibitor to interfere with the binding of amphiphysin with dynamin. DynaMin inhibitory peptide, myristoylated TFA is a membrane-permeant form of the peptide that prevents endocytosis.

Control peptide version of dynamin inhibitory peptide, myristoylated, an inhibitor of the GTPase dynamin that competitively blocks binding of dynamin to amphiphysin, preventing endocytosis. In contrast to dynamin inhibitory peptide, has no significant eff

Cyclin-dependent kinase 2 also known as cell division protein kinase 2. The protein encoded by this gene is a member of the cyclin-dependent kinase family of Ser/Thr protein kinases. This protein kinase is highly similar to the gene products of S. cerevis