peptide m

Peptide M is a synthetic Peptide, 50 aa, derived from streptococcus M protein, containing an additional c-terminal cysteine residue.

Peptide M acetate 是一种合成多肽 (长度为 18 个氨基酸，对应于牛 S 抗原的氨基酸位置303-322: DTNLASSTIIKEGIDKTV)，能够在猴子和 Hartley 豚鼠以及 Lewis 大鼠中诱导实验性自身免疫性葡萄膜炎。

Muscle homing peptide M12 主要结合于肌肉细胞表面蛋白,且能促进肌母细胞对纳米颗粒(NPs)的摄取.该肽通过 N-羟基琥珀酰亚胺酯反应,于其 N-末端α-氨基基团与PLGA-PEG纳米颗粒形成共价连接.

TREM-1 inhibitory peptide M3为一种配体依赖的TREM-1拮抗剂。该化合物能够有效抑制全身及肺部促炎细胞因子与趋化因子的产生，有助于缓解急性肺损伤。

Skeletal muscle-targeted peptide MSP，一种包含7个氨基酸(ASSLNIA)的肌肉靶向肽(MTP)，通过与肌肉的不同结合配体实现对病毒的靶向。该肽主要用于心脏和骨骼肌疾病的研究。

EGFR peptide (myristoylated)是一种合成肽，其氨基酸序列对应于EGFR细胞内区域，能够抑制PKC的活性。

Autocamtide-2-related inhibitory peptide, myristoylated acetate 是CaM 激酶II 抑制剂;是 Autocamtide-2相关抑制肽的增强细胞渗透性衍生物。

Myristoylated PKCε inhibitor peptide（Myr-PKCε-）是一种与肉豆蔻酸偶联、具有细胞渗透性的PKCε蛋白激酶Cε亚型特异性肽抑制剂，它能够降低人脐静脉内皮细胞（HUVECs）的一氧化氮（NO）释放。

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(251634-22-7 free base) 是一种 DynaMin 抑制剂，可干扰两性霉素与 dynamin 的结合。 DynaMin 抑制肽，肉豆蔻酰化 TFA 是肽的膜渗透形式，可防止内吞作用。

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

Autocamtide-2-related inhibitory peptide, myristoylated TFA 是 Autocamtide-2-related inhibitory peptide 烷基化修饰后的形式。 Autocamtide-2-related inhibitory peptide 是高度特异性的、CaMKII 的有效抑制剂，其 IC50值为 40 nM。

ML-18是一种非肽铃蟾肽受体亚型-3 拮抗剂，能够抑制肺癌生长。

The chimeric peptide M35 [galanin (1-13)-bradykinin(2-9) amide] is a high-affinity galanin receptor ligand acting as a galanin receptor antagonist in the rat spinal cord, rat hippocampus and isolated mouse pancreatic islets. The radiolabelled M35 and perf

Actinonin ((-)-Actinonin) is a naturally occurring antibacterial agent produced by Actinomyces and a potent reversible peptide deformylase (PDF) inhibitor with a Ki of 0.28 nM, it also is an apoptosis inducer. Actinonin inhibits aminopeptidase M, aminopeptidase N and leucine aminopeptidase, it also inhibits MMP-1, MMP-3, MMP-8, MMP-9, and hmeprin α with Ki values of 300 nM, 1,700 nM, 190 nM, 330 nM, and 20 nM, respectively. Actinonin has antiproliferative and antitumor activities[1][2][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)

α-Melanocyte-stimulating hormone (α-MSH) is a 13-amino acid peptide hormone produced by post-translational processing of proopiomelanocortin (POMC) in the pituitary gland, as well as in keratinocytes, astrocytes, monocytes, and gastrointestinal cells.1It is an agonist of melanocortin receptor 3 (MC3R) and MC4R that induces cAMP production in Hepa cells expressing the human receptors (EC50s = 0.16 and 56 nM, respectively).2α-MSH (100 pM) reducesS. aureuscolony formation andC. albicansgerm tube formationin vitro.3It inhibits endotoxin-, ceramide-, TNF-α-, or okadaic acid-induced activation of NF-κB in U937 cells.1α-MSH reduces IL-6- or TNF-α-induced ear edema in mice.4It also prevents the development of adjuvant-induced arthritis in rats and increases survival in a mouse model of septic shock. Increased plasma levels of α-MSH are positively correlated with delayed disease progression and reduced death in patients with HIV.1 1.Catania, A., Airaghi, L., Colombo, G., et al.α-melanocyte-stimulating hormone in normal human physiology and disease statesTrends Endocrinol. Metab.11(8)304-308(2000) 2.Miwa, H., Gantz, I., Konda, Y., et al.Structural determinants of the melanocortin peptides required for activation of melanocortin-3 and melanocortin-4 receptorsJ. Pharmacol. Exp. Ther.273(1)367-372(1995) 3.Cutuli, M., Cristiani, S., Lipton, J.M., et al.Antimicrobial effects of a-MSH peptidesJ. Leukoc. Biol.67(2)233-239(2000) 4.Lipton, J.M., Ceriani, G., Macaluso, A., et al.Antiiinflammatory effect of the neuropeptide a-MSH in acute, chronic, and systemic inflammationAnn. N.Y. Acad. Sci.25(741)137-148(1994)

MAT-POS-e194df51-1 是一种非共价、非肽类、口服活性的SARS-CoV-2主蛋白酶 (Mpro) 抑制剂，IC50 值达 37nM。该化合物展现细胞毒性，其在 A549-ACE2-TMPRSS2 和 HeLa-ACE2 细胞线上的 EC50 值分别为 64 nM 和 126 nM。

Calpastatin (184-210), an acetylated synthetic peptide derived from human calpastatin, effectively inhibits the calcium-dependent cysteine proteases, calpain I (µ-calpain) and calpain II (m-calpain), which require micromolar and millimolar calcium concentrations, respectively. Unlike its action on calpains, this 27 amino acid peptide does not inhibit papain (a cysteine protease) or trypsin (a serine protease). Encoded by exon 1B of Ac-calpastatin (184-210), it aligns with a section of inhibitory domain 1, showcasing its specificity and inhibitory function towards calpain enzymes.

PACAP (1-38), a novel neuropeptide isolated from the bovine hypothalamus is more active than vasoactive intestinal peptide (VIP) in stimulating adenylate cyclase (EC50=7 nM). PACAP 1-38 (10-9 M) increased substance P (SP), gastrin releasing peptide (GRP),

Boc-Glu-OBzl is an amino acid building block.1,2It has been used in the synthesis of peptide-based inhibitors of human caspases and human rhinovirus (HRV) 3C protease that have enzyme inhibitory activityin vitro. 1.Garcia-Calvo, M., Peterson, E.P., Leiting, B., et al.Inhibition of human caspases by peptide-based and macromolecular inhibitorsJ. Biol. Chem.273(49)32608-32613(1998) 2.Dragovich, P.S., Webber, S.E., Babine, R.E., et al.Structure-based design, synthesis, and biological evaluation of irreversible human rhinovirus 3C protease inhibitors. 2. peptide structure-activity studiesJ. Med. Chem.41(15)2819-2934(1998)

RWJ-56110 dihydrochloride is a potent, selective, peptide-mimetic inhibitor of PAR-1 activation and internalization (binding IC50=0.44 uM) and shows no effect on PAR-2, PAR-3, or PAR-4. RWJ-56110 dihydrochloride inhibits the aggregation of human platelets induced by both SFLLRN-NH2 (IC50=0.16 μM) and thrombin (IC50=0.34 μM), quite selective relative to U46619 . RWJ-56110 dihydrochloride blocks angiogenesis and blocks the formation of new vessels in vivo. RWJ-56110 dihydrochloride induces cell apoptosis[1][2]. Proteinase-activated receptors (PARs) are a family of G protein-coupled receptors activated by the proteolytic cleavage of their N-terminal extracellular domain, exposing a new amino terminal sequence that functions as a tethered ligand to activate the receptors.RWJ56110 inhibits the aggregation of human platelets induced by both SFLLRN-NH2 (IC50=0.16 μM) and thrombin (IC50=0.34 μM) while being quite selective relative to collagen and the thromboxane mimetic U46619 [1].RWJ-56110 dihydrochloride is fully inhibits thrombin-induced RASMC proliferation with an IC50 value of 3.5 μM. RWJ-56110 dihydrochloride shows blockade of thrombin's action with RASMC calcium mobilization (IC50=0.12 μM), as well as with HMVEC (IC50=0.13 μM) and HASMC calcium mobilization (IC50=0.17 μM)[1].RWJ56110 (0.1-10 μM; 24-96 hours) inhibits endothelial cell growth dose-dependently, with half-maximal inhibitory concentration of RWJ56110 is approximately 10 μM[2].RWJ56110 (0.1-10 μM; 6 hours) inhibits DNA synthesis of endothelial cells in a thymidine incorporation assays. Endothelial cells are in fast-growing state (50-60% confluence), RWJ56110 inhibits cell DNA synthesis in a dose-dependent manner, but when cells that are in the quiescent state (100% confluent), the inhibitory effect of PAR-1 antagonists is much less pronounced[2].RWJ56110 (0.1-10 μM; pretreatment for 15 min) inhibits thrombin-induced Erk1 2 activation in a concentration-dependent manner. However, when endothelial cells are stimulated by FBS (final concentration 4%), it reduces partially the activated levels of Erk1 2[2].RWJ56110 (30 μM; 24 hours) has an inhibitory effect on endothelial cell cycle progression. It reduces the percentage of cells in the S phase, while alterations in the percentages of G1 and G2 M cells are less pronounced[2]. Western Blot Analysis[2] Cell Line: Endothelial cells [1]. Andrade-Gordon, et al.Design, synthesis, and biological characterization of a peptide-mimetic antagonist for a tethered-ligand receptor. oc Natl Acad Sci U S A. 1999 Oct 26;96(22):12257-62. [2]. Panagiota Zania, et al. Blockade of angiogenesis by small molecule antagonists to protease-activated receptor-1: association with endothelial cell growth suppression and induction of apoptosis. J Pharmacol Exp Ther. 2006 Jul;318(1):246-54.

H-Val-Pro-Pro-OH(TFA), a proline peptide derivative from milk, is an ACE inhibitor with IC50 of 9 M.

Kisspeptin-54 is a peptide ligand of the orphan G protein-coupled receptor GPR54 (Kis = 1.81 and 1.45 nM for rat and human receptors, respectively).1 It is a 54 amino acid peptide encoded by the metastasis suppressor gene KISS-1. Kisspeptin-54 induces calcium mobilization in CHO-K1 cells expressing rat and human receptors (EC50s = 1.39 and 5.47 nM, respectively). It also induces arachidonic acid release in CHO cells expressing rat and human GPR54 in a concentration-dependent manner. Kisspeptin-54 (10-1,000 nM) inhibits insulin secretion from isolated mouse pancreatic β-cells in the presence of 2.8 mM, but not 11.1 mM, glucose.2 Kisspeptin-54 (1-5 nmol, i.c.v.) increases serum levels of luteinizing hormone (LH) and follicular stimulating hormone (FSH) in mice, an effect which is reversed by the gonadotropin releasing hormone (GNRH) antagonist acycline.3References1. Kotani, M., Detheux, M., Vandenbogaerde, A.L., et al. The metastasis suppressor gene KiSS-1 encodes kisspeptins, the natural ligands of the orphan G protein-coupled receptor GPR54. J. Biol. Chem. 276(37), 34631-34636 (2001).2. Vikman, J., and Ahrén, B. Inhibitory effect of kisspeptins on insulin secretion from isolated mouse islets. Diabetes Obes. Metab. 11(Suppl 4), 197-201 (2009).3. Gottsch, M.L., Cunningham, M.J., Smith, J.T., et al. A role for kisspeptins in the regulation of gonadotropin secretion in the mouse. Endocrinology 145(9), 4073-4077 (2004). Kisspeptin-54 is a peptide ligand of the orphan G protein-coupled receptor GPR54 (Kis = 1.81 and 1.45 nM for rat and human receptors, respectively).1 It is a 54 amino acid peptide encoded by the metastasis suppressor gene KISS-1. Kisspeptin-54 induces calcium mobilization in CHO-K1 cells expressing rat and human receptors (EC50s = 1.39 and 5.47 nM, respectively). It also induces arachidonic acid release in CHO cells expressing rat and human GPR54 in a concentration-dependent manner. Kisspeptin-54 (10-1,000 nM) inhibits insulin secretion from isolated mouse pancreatic β-cells in the presence of 2.8 mM, but not 11.1 mM, glucose.2 Kisspeptin-54 (1-5 nmol, i.c.v.) increases serum levels of luteinizing hormone (LH) and follicular stimulating hormone (FSH) in mice, an effect which is reversed by the gonadotropin releasing hormone (GNRH) antagonist acycline.3 References1. Kotani, M., Detheux, M., Vandenbogaerde, A.L., et al. The metastasis suppressor gene KiSS-1 encodes kisspeptins, the natural ligands of the orphan G protein-coupled receptor GPR54. J. Biol. Chem. 276(37), 34631-34636 (2001).2. Vikman, J., and Ahrén, B. Inhibitory effect of kisspeptins on insulin secretion from isolated mouse islets. Diabetes Obes. Metab. 11(Suppl 4), 197-201 (2009).3. Gottsch, M.L., Cunningham, M.J., Smith, J.T., et al. A role for kisspeptins in the regulation of gonadotropin secretion in the mouse. Endocrinology 145(9), 4073-4077 (2004).