dpp-3

Picolamine 可作为 DPP-4 的潜在抑制剂。

Talabostat (PT100, Val-boroPro) is a potent, nonselective and orally available dipeptidyl peptidase IV (DPP-IV) inhibitor with a Ki of 0.18 nM. Talabostat is a nonselective DPP-IV inhibitor, inhibiting DPP8 9, FAP, DPP2 and some other DASH family enzymes essentially as potently as it inhibits DPP-IV[1]. Talabostat stimulates the immune system by triggering a proinflammatory form of cell death in monocytes and macrophages known as pyroptosis. The inhibition of two serine proteases, DPP8 and DPP9, activates the proprotein form of caspase-1 independent of the inflammasome adaptor ASC[2]. Talabostat competitively inhibits the dipeptidyl peptidase (DPP) activity of FAP and CD26 DPP-IV, and there is a high-affinity interaction with the catalytic site due to the formation of a complex between Ser630 624 and the boron of talabostat[3]. Talabostat can stimulate immune responses against tumors involving both the innate and adaptive branches of the immune system. In WEHI 164 fibrosarcoma and EL4 and A20 2J lymphoma models, PT-100 causes regression and rejection of tumors. The antitumor effect appears to involve tumor-specific CTL and protective immunological memory. Talabostat treatment of WEHI 164-inoculated mice increases mRNA expression of cytokines and chemokines known to promote T-cell priming and chemoattraction of T cells and innate effector cells[3]. Talabostat treated mice show significant less fibrosis and FAP expression is reduced. Upon PT100 treatment, significant differences in the MMP-12, MIP-1α, and MCP-3 mRNA expression levels in the lungs are also observed. Treatment with PT100 in this murine model of pulmonary fibrosis has an anti-fibro-proliferative effect and increases macrophage activation[4]. [1]. Connolly BA, et al. Dipeptide boronic acid inhibitors of dipeptidyl peptidase IV: determinants of potencyand in vivo efficacy and safety. J Med Chem. 2008 Oct 9;51(19):6005-13. [2]. Okondo MC, et al. DPP8 and DPP9 inhibition induces pro-caspase-1-dependent monocyte and macrophage pyroptosis. Nat Chem Biol. 2017 Jan;13(1):46-53. [3]. Adams S, et al. PT-100, a small molecule dipeptidyl peptidase inhibitor, has potent antitumor effects and augments antibody-mediated cytotoxicity via a novel immune mechanism. Cancer Res. 2004 Aug 1;64(15):5471-80. [4]. Egger C, et al. Effects of the fibroblast activation protein inhibitor, PT100, in a murine model of pulmonary fibrosis. Eur J Pharmacol. 2017 Aug 15;809:64-72.

3-Pyridylacetic acid hydrochloride （3-PAA-HCl）尼克酸的高同系物，是尼古丁（和其它烟草生物碱）的分解产物，还可与胺、醇和羧酸等反应，也可在反应中作为酸催化剂。

DPP，一种含紫檀芪衍生轴向配体的铂(IV)络合物，能够抑制乳腺癌(BC)细胞的JAK2-STAT3通路并显示出抗增殖特性。它通过激活caspase-3和裂解聚ADP-核糖聚合酶诱导细胞凋亡(apoptosis)，同时促进树突状细胞成熟及抗原呈现功能，并已证明体内具有安全性。

DPP-4 inhibitor 3 (Compound 5a) 是一种有效的二肽基肽酶 IV (DPP-IV) 抑制剂，IC50为 0.75 nM。DPP-4 inhibitor 3 具有极好的抗氧化和胰岛素性活性。

Fluostatin A是一种最初从链霉菌中分离出的荧光酮类化合物。它对二肽基肽酶3（DPP-3）的选择性抑制作用优于对DPP-1、DPP-2和DPP-4的抑制作用（IC50s分别为0.44, >100, >100, 和 >100 µg/ml）。

Albiglutide TFA 是一种胰高血糖素样肽GLP-1模拟物，是长效的GLP-1受体激动剂。Albiglutide TFA 可显著降低糖化血红蛋白 (A1C)。Albiglutide TFA 可用于研究 2 型糖尿病 (T2D)。Albiglutide TFA 是由抗DPP-4的GLP-1二聚体与人白蛋白的基因融合产生的。

Albiglutide fragment (GLP-1 (7-36) analog) TFA为Albiglutide活性片段，代表胰高血糖素样肽-1(GLP-1)模拟物，属长效GLP-1受体激动剂。由GLP-1二聚体抗DPP-4特性与人白蛋白基因融合而成，本化合物在降低糖化血红蛋白(A1C)方面表现显著，主要应用于2型糖尿病(T2D)的相关研究。

Pyridin-3-ylmethanamine-d2 是 Pyridin-3-ylmethanamine 的氘代化合物。Pyridin-3-ylmethanamine 的 CAS 号为 3731-52-0。Picolamine可作为 DPP-4 的潜在抑制剂。

Fluostatin B, a fluorenone discovered in Streptomyces, is an inhibitor of dipeptidyl peptidase 3 (DPP-3; IC50= 24 µg/ml).

Kaempferol 3-O-alpha-L-(2, 3-di-Z-p-coumaroyl) rhamnoside (compound 42) 源自悬铃木，属于黄酮醇类化合物。它具有抑制α-淀粉酶和DPP IV 的活性。

Neuropeptide Y (NPY) (3-36) is a C-terminal fragment of NPY, a neuropeptide involved in controlling appetite, blood pressure, cardiac contractility, and intestinal secretion. NPY (3-36) is an endogenous peptide produced by cleavage of NPY by dipeptidyl peptidase 4 (DPP-4). It binds selectively to the NPY receptor Y2 (Ki = 0.41 nM in CHP 234 cells) over the Y1 receptor, where it does not bind at concentrations up to 1 μM. NPY (3-36) (0.1 nM) increases migration of human umbilical vein endothelial cells (HUVECs) by 80% after 12 hours in an in vitro wound closure assay. NPY (3-36) corresponds to residues 3-36 of the human and rat protein sequence.