caspase-12

Tauroursodeoxycholate (UR 906) 是一种天然的高度亲水性的三级胆汁酸。Tauroursodeoxycholate 可用于原发性胆汁性肝硬化 (PBC)、胰岛素抵抗、淀粉样变性、囊性纤维化、胆汁淤滞和肌萎缩性侧索硬化症的研究。

Tauroursodeoxycholate (TUDCA ,Taurolite) dihydrate（牛磺熊去氧胆酸二水合物）是一种水溶性胆汁酸，具有内质网应激抑制、线粒体稳定化和抗凋亡作用，能够显著降低凋亡分子的表达，如Caspase-3和Caspase-12，并抑制ERK，减少内质网应激介导的细胞死亡。

Tauroursodeoxycholate sodium (TUDC) 是一种内质网应激抑制剂。Tauroursodeoxycholate sodium (TUDC) 抑制ERK，显著降低凋亡分子表达，如caspase-3和caspase-12。

Bufotalin (Bufotaline) 是一种从蟾酥中分离的类固醇内酯，可诱导癌细胞凋亡，也诱导内质网应激的激活，具有强大的抗肿瘤活性。

Q-VD-OPH (Quinoline-Val-Asp-Difluorophenoxymethylketone) 是一种具有强效抗凋亡特性的泛半胱天冬酶抑制剂。它可抑制 HIV 感染，能透过血脑屏障。

Taurochenodeoxycholic Acid (12-Deoxycholyltaurine) 是动物胆汁酸的主要生物活性物质之一，可诱导细胞凋亡，具有明显的抗炎和免疫调节作用。

Taurochenodeoxycholic acid sodium (Sodium taurochenodeoxycholate) 是动物胆汁酸的主要生物活性物质之一。它可诱导细胞凋亡，具有抗炎和免疫调节作用。

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.

NVP 231 是一种强效、特异、可逆的神经酰胺激酶抑制剂，IC50值为12 nM，可竞争性地抑制神经酰胺与 CerK 的结合。它通过增加 DNA 片段和 caspase-3 和 caspase-9 的裂解来诱导细胞凋亡。

YHS-12是一种电离性阳离子脂质（pKa = 6.506），可在脂质纳米粒子（LNPs）中封装并传递siRNA和mRNA，用于体外及体内应用。这些LNPs由YHS-12与靶向巨噬细胞的肽CRVLRSGSC组成，主要用于封装针对甲氧西林抗性金黄色葡萄球菌（MRSA）的嵌合抗原受体mRNA以及针对caspase-11的siRNA。此外，这些LNPs能够增强RAW 264.7巨噬细胞及原代小鼠骨髓来源巨噬细胞（BMDMs）清除MRSA的效能。通过静脉注射这些LNPs于环磷酰胺诱导的免疫抑制小鼠的脓毒症模型中，可以显著降低血液中的细菌数量并提高生存率。

ERK1 2 inhibitor 12 (compound 76.3) 是一种可以抑制 ERK 介导的 caspase-9 和 p90Rsk-1 激酶磷酸化的ERK1 2抑制剂。ERK1 2 inhibitor 12 具有抗癌活性，适用于癌症研究。

FL3 is a novel potent eIF4F inhibitor, it induces the death of cancer cells by an original mechanism that involves the apoptosis-inducing factor and caspase 12.

2-chloro Palmitic acid is a monochlorinated form of palmitic acid . It is produced in a myeloperoxidase (MPO) and time-dependent manner in neutrophils stimulated by phorbol 12-myristate 13-acetate . 2-chloro Palmitic acid (10 μM) induces neutrophil extracellular trap (NET) formation (NETosis) in human neutrophils, increasing DNA release from neutrophils, colocalization of MPO with extracellular DNA (ecDNA), and trapping of E. coli. It increases COX-2 protein levels in human coronary artery endothelial cells (HCAECs) when used at a concentration of 50 μM and increases production of P-selectin, von Willebrand factor, and angiopoietin-2 in HCAECs, as well as neutrophil and platelet adherence, when used at a concentration of 10 μM. 2-chloro Palmitic acid (10-50 μM) also induces apoptosis in THP-1 cells and primary human monocytes and increases caspase-3 activity in THP-1 cells.

Nemorosone is a polycyclic polyprenylated acylphloroglucinol (PPAP) originally isolated from C. rosea that has antiproliferative properties.1 Nemorosone inhibits growth of NB69, Kelly, SK-N-AS, and LAN-1 neuroblastoma cells (IC50s = 3.1-6.3 μM), including several drug-resistant clones, but not MRC-5 human embryonic fibroblasts (IC50 = >40 μM).2 It increases DNA fragmentation in LAN-1 cells in a dose-dependent manner, and decreases N-Myc protein levels and phosphorylation of ERK1 2 by MEK1 2. Nemorosone also inhibits growth of Capan-1, AsPC-1, and MIA-PaCa-2 pancreatic cancer cells (IC50s = 4.5-5.0 μM following a 72-hour treatment) but not human dermal and foreskin fibroblasts (IC50s = >35 μM).1 It induces apoptosis, abolishes the mitochondrial membrane potential, and increases cytosolic calcium concentration in pancreatic cancer cells in a dose-dependent manner. Nemorosone activates the caspase cascade in a dose-dependent manner and inhibits cell cycle progression, increasing the proportion of cells in the G0 G1 phase, in both neuroblastoma and pancreatic cancer cells.1,2 Nemorosone (50 mg kg, i.p., per day) also reduces tumor growth in an MIA-PaCa-2 mouse xenograft model.3References1. Holtrup, F., Bauer, A., Fellenberg, K., et al. Microarray analysis of nemorosone-induced cytotoxic effects on pancreatic cancer cells reveals activation of the unfolded protein response (UPR). Br. J. Pharmacol. 162(5), 1045-1059 (2011).2. Díaz-Carballo, D., Malak, S., Bardenheuer, W., et al. Cytotoxic activity of nemorosone in neuroblastoma cells. J. Cell. Mol. Med. 12(6B), 2598-2608 (2008).3. Wold, R.J., Hilger, R.A., Hoheisel, J.D., et al. In vivo activity and pharmacokinetics of nemorosone on pancreatic cancer xenografts. PLoS One 8(9), e74555 (2013). Nemorosone is a polycyclic polyprenylated acylphloroglucinol (PPAP) originally isolated from C. rosea that has antiproliferative properties.1 Nemorosone inhibits growth of NB69, Kelly, SK-N-AS, and LAN-1 neuroblastoma cells (IC50s = 3.1-6.3 μM), including several drug-resistant clones, but not MRC-5 human embryonic fibroblasts (IC50 = >40 μM).2 It increases DNA fragmentation in LAN-1 cells in a dose-dependent manner, and decreases N-Myc protein levels and phosphorylation of ERK1 2 by MEK1 2. Nemorosone also inhibits growth of Capan-1, AsPC-1, and MIA-PaCa-2 pancreatic cancer cells (IC50s = 4.5-5.0 μM following a 72-hour treatment) but not human dermal and foreskin fibroblasts (IC50s = >35 μM).1 It induces apoptosis, abolishes the mitochondrial membrane potential, and increases cytosolic calcium concentration in pancreatic cancer cells in a dose-dependent manner. Nemorosone activates the caspase cascade in a dose-dependent manner and inhibits cell cycle progression, increasing the proportion of cells in the G0 G1 phase, in both neuroblastoma and pancreatic cancer cells.1,2 Nemorosone (50 mg kg, i.p., per day) also reduces tumor growth in an MIA-PaCa-2 mouse xenograft model.3 References1. Holtrup, F., Bauer, A., Fellenberg, K., et al. Microarray analysis of nemorosone-induced cytotoxic effects on pancreatic cancer cells reveals activation of the unfolded protein response (UPR). Br. J. Pharmacol. 162(5), 1045-1059 (2011).2. Díaz-Carballo, D., Malak, S., Bardenheuer, W., et al. Cytotoxic activity of nemorosone in neuroblastoma cells. J. Cell. Mol. Med. 12(6B), 2598-2608 (2008).3. Wold, R.J., Hilger, R.A., Hoheisel, J.D., et al. In vivo activity and pharmacokinetics of nemorosone on pancreatic cancer xenografts. PLoS One 8(9), e74555 (2013).

Taurodeoxycholic acid (Taurodeoxychloic acid) 是脱氧胆酸的胆汁酸牛磺酸共轭物，是一种人体代谢物，可稳定线粒体膜，减少自由基形成。Taurodeoxycholic acid 通过阻断钙介导的凋亡通路以及 Caspase-12 激活来抑制凋亡 (apoptosis)。Taurodeoxycholic acid具有神经保护活性，可用于研究 3-硝基丙酸诱导或稳定遗传的亨廷顿舞蹈病 (HD) 。

CTL-06是一种Fatty Acid Synthase (FASN)抑制剂，具有3 μM的IC50，能够诱发细胞凋亡。CTL-12导致细胞周期在Sub-G1 S期停滞，并增加caspase-9和凋亡标志物Bax的表达，减少抗凋亡标志物Bcl-xL的表达。此外，CTL-12通过抑制脂肪酸的从头合成，剥夺肿瘤细胞代谢所需，主要用于乳腺癌和结直肠癌的研究。

CTL-12是一种Fatty Acid Synthase (FASN)抑制剂（IC50: 2.5 μM），能够诱导apoptosis。它使细胞周期在Sub-G1 S期停滞并增加caspase-9和凋亡标志物Bax的表达，同时减少抗凋亡标志物Bcl-xL的水平。CTL-12通过抑制de novo脂肪酸合成，切断了肿瘤细胞的代谢需求，是乳腺癌和结直肠癌研究中的重要工具。

BDS-I，又名降血物质，源自苏卡达银莲花的海洋毒素。它作为钾通道特异性抑制剂，针对Kv3.4。BDS-I能够抑制由Aβ1-42诱导的Kv3.4活性增强，减少caspase-3的激活，阻止NGF诱导的PC-12细胞分化以及异常核形态的出现，并可逆转Aβ肽引发的细胞死亡。

Taurohyodeoxycholic acid sodium salt (Sodium taurohyodeoxycholate hydrate) 通过阻断钙介导的细胞凋亡途径以及 Caspase-12 活化来防止细胞凋亡

Apoptosisinducer 20 (12) 作用于细胞周期的G2 M阶段,通过激活caspase-3 7来引起细胞凋亡(apoptosis),特别是在M阶段阻塞时.此化合物为一种新型吲哚类苯磺酰胺化合物,展示了对多种癌细胞的抗增殖能力,是研发新型抗有丝分裂药物的有望候选.

Taurodeoxycholic acid sodium hydrate (Sodium taurodeoxycholate monohydrate) 通过阻断钙介导的凋亡通路和 Caspase-12的活化来阻止细胞凋亡。它可用于原发性胆汁性肝硬化、胰岛素抵抗、淀粉样变性、囊性纤维化、胆汁淤积和肌萎缩侧索硬化症。

4,4′-Secalonic acid D (Compound 12) 是一种抑制PARP1的化合物。通过抑制PARP1，该化合物诱导ROS积累和DNA损伤，并激活caspase-3 GSDME通路，从而引发肿瘤细胞的凋亡 (apoptosis) 和焦亡 (pyroptosis)。4,4′-Secalonic acid D 具有显著的抗肿瘤活性。

Z-ATAD-FMK 是一种caspase-12的抑制剂。它通过抑制caspase-12的活性来减少caspase-9的活性，从而阻止内质网应激引发的细胞凋亡。

Met-12 是一种小肽抑制剂，作用于Fas受体，可抑制由Fas受体介导的光感受器细胞凋亡 (apoptosis)，并减少Caspase的激活。Met-12 可应用于光感受器保护剂的研究。