ras inhibitory peptide

Son of sevenless homolog 1 (Sos1) is a guanine nucleotide exchange factor (GEF) that directs the exchange of Ras-GDP to Ras-GTP by binding to SH3 domains of the growth factor receptor-bound protein 2 (Grb2), leading to the activation of ERK. Ras inhibitory peptide is a synthetic peptide that contains the sequence PVPPR, which corresponds to a region within human Sos1 that interacts with an SH3 domain of Grb2. It specifically blocks the interaction of the GEF with Grb2, preventing an interaction that is essential for Ras activation by receptor tyrosine kinases, including epidermal growth factor receptor.

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.

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.

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.

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

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 is a potent and highly specific inhibitor of CaMKII, with an IC50 of 40 nM.

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].

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.

Compound CP2, also known as SPSB2-iNOS inhibitory cyclic peptide-2, serves as an inhibitor disrupting the interaction between SPRY domain and SOCS-box protein 2 (SPSB2) and iNOS. It binds to the SPSB2 on the iNOS site with an affinity (K D) of 21 nM. This peptide is characterized by its resistance to reduction and oxidative stability [1].

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].

[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].

Renin inhibitory peptide, statine is a effective, specific statine-containing renin inhibitor.

SPSB2-iNOS inhibitory cyclic peptide-1, an inhibitor for the interaction between the SPRY domain and SOCS-box protein 2 (SPSB2) and iNOS, binds SPSB2 at the iNOS site with a K D of 4.4 nM. It is resistant to proteases pepsin, trypsin, and α-chymotrypsin and remains stable in human plasma and oxidative environments [1].

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].

Renin inhibitory peptide is an analog of angiotensinogen.

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

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.

CaMKII inhibitory peptide KIIN serves as a potent inhibitor of CaMKII [1] [2].

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].

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.

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

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].

**SPSB2-iNOS inhibitory cyclic peptide-3 (Compound CP3)** is an inhibitor that disrupts the interaction between SPRY domain and SOCS-box protein 2 (SPSB2) and iNOS, by binding to SPSB2 at the iNOS site with a K D of 7 nM [1].

Fusion Inhibitory Peptide (Z-D-Phe-Phe-Gly-OH, FIP, Virus Replication Inhibitory Peptide) effectively blocks virus replication by inhibiting the membrane fusion activity of a specific viral glycoprotein [1].

Cdk2 Cyclin Inhibitory Peptide II (Tat-LDL), a CDK2 inhibitor, exhibits dose-dependent cytotoxic effects on U2OS osteosarcoma cells [1].

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

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

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.

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].

GF9 (Human TREM-1(213-221)), a TREM-1 inhibitory peptide, effectively mitigates the severe inflammation associated with rheumatoid arthritis (RA) [1]. This nonapeptide functions independently of ligands to inhibit TREM-1.

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.

KRPEP-2D acetate was identified as a K-Ras(G12D) selective inhibitory peptide against the G12D mutant of K-Ras, which is a key member of the Ras protein family and an attractive cancer therapeutic target.