amino-terminal

EPI-001 is an androgen receptor N-terminal domain antagonist with IC50 of ～6 μM and a selective PPAR-gamma modulator.

Diaminopimelic acid or DAPA is a lysine-like amino acid derivative that is a key component of the bacterial cell wall. DAPA is incorporated or integrated into peptidoglycan of gram negative bacteria and is the attachment point for Braun's lipoprotein (BLP or Murein Lipoprotein). BLP is found in gram-negative cell walls and is one of the most abundant membrane proteins. BLP is bound at its C-terminal end (a lysine) by a covalent bond to the peptidoglycan layer (specifically to diaminopimelic acid molecules) and is embedded in the outer membrane by its hydrophobic head (a cysteine with lipids attached). BLP tightly links the two layers and provides structural integrity to the bacterial outer membrane. Diaminopimelic acid can be found in human urine or feces due to the lysis or enzymatic breakdown of gram negative gut microbes.

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.

Butanoic acid, 4-[[2-(2,6-dioxo-3-piperidinyl)-2,3-dihydro-1,3-dioxo-1H-isoindol-4-yl]amino]- (4-[[2-(2,6-dioxopiperidin-3-yl)-1,3-dioxoisoindol-4-yl]amino]butanoic acid) is a Cereblon ligand with alkyl linker and terminal acid for onward chemistry.

gamma-preprotachykinin amide (72-92) acetate is a 21 amino acid peptide belonging to the tachykinin (TK) family and including neurokinin A (NKA) in its C-terminal sequence. gamma-preprotachykinin amide (72-92) acetate possesses higher affinity than NKA for central NK-2 receptors; it shows lower affinity for NK-1 receptors, however, it potently stimulates salivary secretion, which is mediated by NK-1 receptor activation.

N-(Amino-PEG5)-N-bis(PEG4-acid) is a PEG-based PROTAC linker used for synthesizing PROTACs, consisting of an amino group and two terminal carboxylic acids[1].

15-Aminopentadecanoic acid serves as a linker in PROTAC synthesis. It features an alkane chain with terminal carboxylic acid and amino groups. The amino group (NH2) can react with carboxylic acids, activated NHS esters, and carbonyls (ketones, aldehydes). The terminal carboxylic acid can form stable amide bonds with the primary amine group of activated NHS esters.

16-Aminohexadecanoic acid is an alkyl chain compound characterized by terminal carboxylic acid and amino groups. It serves as a PROTAC linker in PROTAC synthesis. The amino group (NH2) can react with carboxylic acids, activated NHS esters, and carbonyl groups (ketones, aldehydes). The terminal carboxylic acid can form stable amide bonds by reacting with primary amines of activated NHS esters.

10-Aminodecanoic acid is an alkane chain featuring terminal carboxylic acid and amino groups. This compound serves as a PROTAC linker in PROTAC synthesis and other conjugation applications. The amino group (NH2) can react with carboxylic acids, activated NHS esters, and carbonyls (ketones, aldehydes), while the terminal carboxylic acid can react with primary amines of activated NHS esters to form stable amide bonds.

tert-Butyl (10-aminodecyl)carbamate (1-Boc-1,10-diaminodecane) serves as a PROTAC linker in the synthesis of PROTACs and other binding applications. This compound contains an alkane chain with a terminal amine and a Boc-protected amino group. The amine group can react with carboxylic acids, activated NHS esters, and carbonyls (ketones and aldehydes). The Boc group can be removed under mild acidic conditions to yield a free amine.

9-Aminononanoic acid can serve as a PROTAC linker and in other conjugates for PROTAC synthesis. This compound consists of an alkyl chain featuring terminal carboxylic acid and amino groups. The amino group (NH2) can react with carboxylic acids, activated NHS esters, carbonyls (ketones, aldehydes), among others. The terminal carboxylic acid is able to react with primary amines of activated NHS esters to form stable amide bonds.

tert-Butyl (9-aminononyl)carbamate is an alkane chain featuring a terminal amine and a Boc-protected amino group. It serves as a PROTAC linker in the synthesis of PROTACs and various coupling applications. The amine can react with carboxylic acids, activated NHS esters, and carbonyl groups (ketones, aldehydes). The Boc group can be deprotected under mild acidic conditions to form a free amine.

N-Boc-undecane-1,11-diamine is an alkane chain featuring terminal amine and Boc-protected amino groups. It serves as a PROTAC linker in PROTAC synthesis and other conjugation applications. The amine group can react with carboxylic acids, activated NHS esters, and carbonyl groups (ketones, aldehydes). The Boc group can be deprotected under mild acidic conditions to yield a free amine.

Emd 55450 is a synthetic renin antagonist. It is an analog of EMD 55068 with terminal amino group blocked by benzyloxycarbonyl group.

Hypusine is an N-terminal amino alcohol derivative of Lys occurring in bovine brain &

Obestatin is a 23 amino acid peptide hormone with a conserved C-terminal glycine residue and amidation site that is formed by cleavage of the ghrelin and obestatin prepropeptide.1It binds to the orphan receptor GPR39 (Kd= 1 nM) and stimulates cAMP production in CHO and HEK293 cells overexpressing human GPR39. Obestatin inhibits contraction of isolated mouse jejunum muscle strips induced by ghrelin .In vivo, obestatin (12.5-1,000 nmol/kg) suppresses food intake in a time- and dose-dependent manner and reduces body weight gain and gastric emptying in mice. Obestatin (0.22 g per animal) also reduces food intake and glucose response without affecting plasma insulin responses in fasted high-fat diet fed mice.2 1.Zhang, J.V., Ren, P.C., Avsian-Kretchmer, O., et al.Obestatin, a peptide encoded by the ghrelin gene, opposes ghrelin's effects on food intakeScience310(5750)996-999(2005) 2.Subasinghage, A.P., Green, B.D., Flatt, P.R., et al.Metabolic and structural properties of human obestatin {1-23} and two fragment peptidesPeptides31(9)1697-1705(2010)

Protein kinase C (PKC ) is a calcium-independent, phospholipid- and diacylglycerol-dependent serine/threonine kinase involved in diverse signaling pathways, including those involved in neuronal signaling, cytoskeletal function, and inflammation.[1] PKC inhibitor peptide is a synthetic peptide corresponding to an amino acid sequence found in the amino terminal C2 domain of most mammalian forms of PKC .[2] It selectively and reversibly inhibits the translocation of PKC to intracellular membranes, blocking activation.[2] PKC inhibitor peptide is commonly used in cells to evaluate the role of PKC in various cellular responses.[3],[4],[5]

PAR2 (1-6) amide is a synthetic peptide agonist of proteinase-activated receptor 2 (PAR2) that corresponds to residues 1-6 of the amino terminal tethered ligand sequence of human PAR2 and residues 37-42 of the full-length sequence.1It binds to NCTC 2544 cells expressing human PAR2 (Ki= 9.64 μM in a radioligand binding assay) and induces calcium mobilization in the same cells (EC50= 0.075 μM).2PAR2 (1-6) amide (100 μM) reduces colony formation of A549 lung cancer cells.1It induces superoxide production and degranulation in isolated human eosinophils when used at a concentration of 500 μM.3PAR2 (1-6) amide (5 μmol/kg) induces tear secretion in rats when used in combination with amastatin .4 1.Bohm, S.K., Kong, W., Bromme, D., et al.Molecular cloning, expression and potential functions of the human proteinase-activated receptor-2Biochem. J.314(Pt 3)1009-1016(1996) 2.Kanke, T., Ishiwata, H., Kabeya, M., et al.Binding of a highly potent protease-activated receptor-2 (PAR2) activating peptide, [3H]2-furoyl-LIGRL-NH2, to human PAR2Br. J. Pharmacol.145(2)255-263(2005) 3.Miike, S., McWilliam, A.S., and Kita, H.Trypsin induces activation and inflammatory mediator release from human eosinophils through protease-activated receptor-2J. Immunol.167(11)6615-6622(2001) 4.Nishikawa, H., Kawai, K., Tanaka, M., et al.Protease-activated receptor-2 (PAR-2)-related peptides induce tear secretion in rats: Involvement of PAR-2 and non-PAR-2 mechanismsJ. Pharmacol. Exp. Ther.312(2)324-331(2005)

PAR2 (1-6) is a synthetic peptide agonist of proteinase-activated receptor 2 (PAR2) that corresponds to residues 1-6 of the amino terminal tethered ligand sequence of mouse and rat PAR2. It also corresponds to residues 39-44 and 37-42 of the mouse and rat full-length sequences, respectively. PAR2 (1-6) induces relaxation in precontracted rat arteries in a concentration-dependent manner, an effect that can be reduced by the nitric oxide synthase inhibitor L-NNA . It inhibits keratinocyte growth in the presence and absence of growth factors. PAR2 (1-6) inhibits LPS-induced pulmonary neutrophil influx and increases in matrix metalloproteinase-2 (MMP-2) activity in mice.

Histone H3 (21-44)-GK-biotin is a peptide fragment of histone H3 that corresponds to amino acid residues 22-45 of the human histone H3.1 and 3.2 sequences and is biotinylated via a C-terminal GK linker. Histone H3 (21-44) contains a lysine residue at position 23 that is subject to acetylation, an arginine at position 26 subject to methylation, and a serine at position 28 subject to phosphorylation, as well as lysine residues at positions 27 and 36 that are subject to methylation and acetylation. Histone H3 (21-44)-GK-biotin has been used as a substrate for the primate-specific histone methyltransferase PR domain-containing protein 7 (PRDM7) to determine substrate specificity.

Histone H2B (108-125) is a peptide fragment of histone H2B that corresponds to amino acid residues 109-126 of the human histone H2B sequence. It contains an N-terminal biotinylated lysine followed by a tryptophan linker. Histone H2B can be modified by addition of an O-linked N-acetylglucosamine (GlcNAc) moiety to the serine residue at position 112, which promotes monoubiquitination of the lysine at position 120.1 Both of these modifications are associated with active transcription. Histone H2B also has lysine residues at positions 108, 116, and 120 that are subject to acetylation.2References1. Fujiki, R., Hashiba, W., Sekine, H., et al. GlcNAcylation of histone H2B facilitates its monoubiquitination. Nature 480(7378), 557-560 (2011).2. Portela, A., and Esteller, M. Epigenetic modifications and human disease. Nat. Biotechnol. 28(10), 1057-1068 (2010). Histone H2B (108-125) is a peptide fragment of histone H2B that corresponds to amino acid residues 109-126 of the human histone H2B sequence. It contains an N-terminal biotinylated lysine followed by a tryptophan linker. Histone H2B can be modified by addition of an O-linked N-acetylglucosamine (GlcNAc) moiety to the serine residue at position 112, which promotes monoubiquitination of the lysine at position 120.1 Both of these modifications are associated with active transcription. Histone H2B also has lysine residues at positions 108, 116, and 120 that are subject to acetylation.2 References1. Fujiki, R., Hashiba, W., Sekine, H., et al. GlcNAcylation of histone H2B facilitates its monoubiquitination. Nature 480(7378), 557-560 (2011).2. Portela, A., and Esteller, M. Epigenetic modifications and human disease. Nat. Biotechnol. 28(10), 1057-1068 (2010).

High affinity JNK inhibitor (Ki values are 25-50 nM). Inhibits JNK via competitive binding of the ATP-binding site of active, phosphorylated JNK. Exhibits > 40-fold selectivity for JNK over p38, ERK, IKK2, protein kinase C, Lck and ZAP70. Hepatoprotective. Also inhibits HCMV replication. Uehara et al (2004) c-Jun N-terminal kinase mediates hepatic injury after rat liver transplantation. Transplantation. 78 324 PMID:15316358 |Uehara et al (2005) JNK mediates hepatic ischemia reperfusion injury. J.Hepatol. 42 850 PMID:15885356 |Ma et al (2007) A pathogenic role for c-Jun amino-terminal kinase signaling in renal fibrosis and tubular cell apoptosis. J.Am.Soc.Nephrol. 18 472 PMID:17202416 |Ma et al (2009) Blockade of the c-Jun amino terminal kinase prevents crescent formation and halts established anti-GBM glomerulonephritis in the rat. Lab.Invest. 89 470 PMID:19188913 |Zhang et al (2015) The c-Jun N-terminal kinase inhibitor SP600125 inhibits human cytomegalovirus replication. J.Med.Virol. 87 2135 PMID:26058558 |Vasilevskaya et al (2015) Inhibition of JNK sensitizes hypoxic colon cancer cells to DNA-damaging agents. Clin.Cancer.Res. 21 4143 PMID:26023085

RWJ-56110 dihydrochloride is a potent, selective, peptide-mimetic inhibitor of PAR-1 activation and internalization (binding IC50=0.44 μM), showing no effect on PAR-2, PAR-3, or PAR-4. It inhibits the aggregation of human platelets induced by SFLLRN-NH2 (IC50=0.16 μM) and thrombin (IC50=0.34 μM), with high selectivity relative to U46619. RWJ-56110 dihydrochloride also blocks angiogenesis and the formation of new vessels in vivo, and induces cell apoptosis[1][2].

Human ACE2 receptor-derived 23-amino acid peptide. Binds receptor binding domain (RBD) of insect-derived SARS-CoV-2 spike protein (KD = 1.3 μM for N-terminal biotinylated, insect-derived spike protein RBD; see Zhang et al preprint publication). Please note - unpublished, in-house data suggests approximately 75-fold lower affinity for insect-derived SARS-CoV-2 RBD than reported by Zhang et al.