dpp-3

Compound 5a, also known as DPP-4 inhibitor 3, is a powerful dipeptidyl peptidase IV (DPP-IV) inhibitor, demonstrating an IC50 value of 0.75 nM. It exhibits outstanding antioxidant and insulinotropic activity [1].

Ru(dpp)3(PF6)2 is a complex containing the metal ruthenium (Ru) and acts as a chemiluminescent oxygen probe. The compound [Ru(dpp)3]2+ emits light via metal-to-ligand charge transfer (MLCT), where charge transfers from Ru to the ligand, resulting in fluorescence. This fluorescence is effectively quenched by molecular oxygen, making Ru(dpp)3(PF6)2 widely utilized in biosensors, environmental monitoring, and materials science. Additionally, the ability of Ru2+ in Ru(dpp)3(PF6)2 to oxidize to Ru3+ is instrumental in the design and development of solid-state electroluminescent cells.

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) is a high homologue of niacin. It is a decomposition product of nicotine (and other tobacco alkaloids). It can also react with amines, alcohols and carboxylic acids, and can also act as an acid in the reaction. catalyst.

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.

Albiglutide TFA, a glucagon-like peptide (GLP)-1 mimetic, is a long acting GLP-1 receptor agonist. Albiglutide TFA significantly reduces glycosylated hemoglobin (A1C). Albiglutide TFA can be used for type 2 diabetes (T2D) research. Albiglutide TFA is generated by the genetic fusion of a DPP-4-resistant GLP-1 dimer to human albumin [1] [2] [3] .

Albiglutide fragment (GLP-1 (7-36) analog) TFA represents a biologically active segment of Albiglutide, resistant to DPP-4 degradation due to its structure as a GLP-1 analog. It functions as a long-acting agonist of the GLP-1 receptor, derived from a fusion of a GLP-1 dimer with the human albumin gene. Clinically, this compound demonstrates a pronounced reduction in glycosylated hemoglobin (A1C) levels, rendering it a valuable therapeutic in type 2 diabetes (T2D) research [1] [2] [3] [4].

DPP, a Platinum(IV) complex with a pterostilbene-derived axial ligand, inhibits the JAK2-STAT3 pathway in breast cancer (BC) cells, demonstrating antiproliferative activity. It activates caspase-3 and cleaved poly ADP-ribose polymerase, inducing apoptosis. Furthermore, DPP enhances the maturation and antigen presentation of dendritic cells and exhibits in vivo safety [1].

Fluostatin A, a fluorenone compound initially isolated from Streptomyces, demonstrates selective inhibition towards dipeptidyl peptidase 3 (DPP-3) compared to DPP-1, DPP-2, and DPP-4 with IC50 values of 0.44 µg/ml for DPP-3 and over 100 µg/ml for the others, respectively.

Pyridin-3-ylmethanamine-d2 is a deuterated compound of Pyridin-3-ylmethanamine. Pyridin-3-ylmethanamine has a CAS number of 3731-52-0. Picolamine acts as a potential inhibitor of DPP-4.

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), a flavonol extracted from Platanus Occidentalis, functions as an inhibitor of alpha-amylase and DPP IV [1].