increases apoptosis

JGB1741 (ILS-JGB-1741) 是一种有效的选择性 SIRT1 抑制剂，IC50 为 15 μM。 JGB1741 调节 Bax Bcl2 比率、细胞色素 c 释放和 PARP 裂解并增加乙酰化 p53 水平，导致 p53 介导的细胞凋亡。 JGB1741可用于乳腺癌研究。

Musk ketone 可诱导癌细胞生长抑制和凋亡。它增加谷胱甘肽 S-转移酶的活性，因此可能被证明是有用的癌症化学保护剂。

Penicillamine (Artamine) 是一种 penicillin 的代谢降解产物，是一种螯合剂，可作用于威尔逊氏病。

Protosappanin B (Q-100961) 是从苏木中提取的一种多酚类天然产物，具有抗肿瘤作用。它通过激活 MDM2 依赖性泛素化过程诱导 p53 蛋白降解。它显著提高细胞活力，抑制细胞凋亡并上调生长相关蛋白 43 的表达。

2,5-dimethyl Celecoxib 是塞来昔布衍生物和微粒体前列腺素 E 合酶 1 (mPGES-1) 的靶向抑制剂，mPGES-1 是炎症介质 PGE2 合成途径中的关键酶。

DS-7423 是PI3K 和mTOR 的有效抑制剂，抑制PI3Kα 和 mTOR 的IC50分别为15.6 nM 和 34.9 nM。DS-7423表现出抗癌活性。

Ara-G 是一种脱氧鸟苷 (GdR) 类似物和核苷类似物，可被 T 淋巴谱系细胞迅速转化为其相应的阿拉伯糖基鸟嘌呤核苷酸三磷酸 (araGTP)，从而抑制 DNA 合成和对 T 淋巴母细胞的选择性体外毒性细胞系以及来自 T 细胞急性淋巴细胞白血病 (ALL) 患者的新鲜分离的白血病细胞。

MAO-IN-M30 dihydrochloride (M 30 dihydrochloride) 是一种口服活性，可通过血脑屏障的，脑选择性不可逆 MAO-A (IC50=37 nM) 和 MAO-B (IC50=57 nM) 抑制剂。MAO-IN-M30 dihydrochloride 是有效的铁螯合剂、自由基清除剂。MAO-IN-M30 dihydrochloride 对 Dexamethasone 诱导的脑细胞凋亡具有神经保护作用。MAO-IN-M30 dihydrochloride 在 MPTP 和 lactacystin 帕金森病模型中也显示出神经恢复活性。

Momordin Ic (Momordin 1c) 是山茱萸的主要皂苷成分，通过氧化应激调控线粒体功能障碍诱导细胞凋亡，具有抗癌活性。

Kirenol (Kirel) 是分离自 Siegesbeckia orientalis 中的，具有抗氧化、抗炎、抗过敏、抗关节炎活性，可用于缓解疼痛的研究。

Niraparib hydrochloride (MK-4827 hydrochloride) 是一种具有口服活性的PARP1和PARP2抑制剂，IC50值分别为 3.8 nM 和 2.1 nM。它抑制 DNA 损伤修复，诱导凋亡并具有抗肿瘤活性。

Z-LEHD-FMK 是一种具有选择性和有效性的 caspase-9 抑制剂，可防减轻再灌注损伤，减缓细胞凋亡。Z-LEHD-FMK 具有抗肿瘤和神经保护活性，可提高体外生产的水牛 （Bubalus bubalis） 植入前胚胎的产量并改变细胞应激反应。

EOAI3402143 是一种去泛素化酶抑制剂，以剂量依赖性抑制 Usp9x/Usp24和 Usp5，增加肿瘤细胞凋亡。

5,7-Dihydroxychromone (5,7-Dihydroxy-4H-Chromen-4-One) 是一种Cudrania tricuspidata 的提取物，通过激活 Nrf2 ARE 信号对 6-OHDA 诱导的氧化应激和细胞凋亡发挥神经保护作用。它抑制 6-OHDA 诱导的 SH-SY5Y 细胞中活化的caspase-3，caspase-9以及切割的PARP 表达。

CAY10526 (BTH) 是 mPGES-1 的选择性抑制剂，可抑制 NF-κB 信号通路。

Coptisine (Coptisin) 是一种从黄连中分离到的生物碱，是非竞争性的IDO 抑制剂，Ki=为 5.8 μM，IC50=6.3 μM。

4-Deoxypyridoxine hydrochloride 通过抑制 S1P 裂解酶 (SPL) 活性来抑制细胞内 S1P 的降解，与 S1P 一样，减少化学诱导的胰岛素瘤细胞系的细胞凋亡。

MTP 131 acetate 是一种小的线粒体靶向四肽。

STR-V-53 是一个 HDAC 抑制剂 (IC50 in nM)，通过抑制酶的活性增加肿瘤细胞中的组蛋白乙酰化，调控基因表达，抑制肿瘤生长并诱导细胞凋亡。

PI3Kα-IN-8 是 PI3Kα 的选择性抑制剂 (IC50: 0.012 μM)。PI3Kα-IN-8 能够提高细胞内活性氧（reactive oxygen species）水平，降低线粒体膜电位，诱导细胞凋亡（apoptosis）。

KRAS4b-PDEδ stabilizer C19 is a stabilizer of the KRAS4b-PDEδ complex which decreases the proliferation of colorectal cancer cells, and increases apoptosis via decreased activation of oncogenic KRAS4b signaling.

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).

Antitumor agent-60 是有效的抗肿瘤药物，靶向RAS-RAF 信号通路，可与CRAF 结合 (Kd: 721.3 nM)。Antitumor agent-60 能增加癌细胞中p53和ROS 水平，使细胞核呈椭圆形和不规则形态。Antitumor agent-60 够将细胞的细胞周期阻滞在 G2/M 期，并诱导细胞凋亡 (apoptosis)。在 A549 肿瘤移植模型中，Antitumor agent-60 具有一定的抑制肿瘤生长能力。

2-deoxy-D-Glucose-13C6is intended for use as an internal standard for the quantification of 2-deoxy-D-glucose by GC- or LC-MS. 2-deoxy-D-Glucose is a glucose antimetabolite and an inhibitor of glycolysis.1,2It inhibits hexokinase, the enzyme that converts glucose to glucose-6-phosphate, as well as phosphoglucose isomerase, the enzyme that converts glucose-6-phosphate to fructose-6-phosphate.32-deoxy-D-Glucose (16 mM) induces apoptosis in SK-BR-3 cells, as well as inhibits the growth of 143B osteosarcoma cells cultured under hypoxic conditions when used at a concentration of 2 mg ml.4,5In vivo, 2-deoxy-D-glucose (500 mg kg) reduces tumor growth in 143B osteosarcoma and MV522 non-small cell lung cancer mouse xenograft models when used alone or in combination with doxorubicin or paclitaxel .6 1.Kang, H.T., and Hwang, E.S.2-Deoxyglucose: An anticancer and antiviral therapeutic, but not any more a low glucose mimeticLife Sci.78(12)1392-1399(2006) 2.Aft, R.L., Zhang, F.W., and Gius, D.Evaluation of 2-deoxy-D-glucose as a chemotherapeutic agent: Mechanism of cell deathBr. J. Cancer87(7)805-812(2002) 3.Ralser, M., Wamelink, M.M., Struys, E.A., et al.A catabolic block does not sufficiently explain how 2-deoxy-D-glucose inhibits cell growthProc. Natl. Acad. Sci. USA105(46)17807-17811(2008) 4.Liu, H., Savaraj, N., Priebe, W., et al.Hypoxia increases tumor cell sensitivity to glycolytic inhibitors: A strategy for solid tumor therapy (Model C)Biochem. Pharmacol.64(12)1745-1751(2002) 5.Zhang, X.D., Deslandes, E., Villedieu, M., et al.Effect of 2-deoxy-D-glucose on various malignant cell lines in vitroAnticancer Res.26(5A)3561-3566(2006) 6.Maschek, G., Savaraj, N., Priebe, W., et al.2-deoxy-D-glucose increases the efficacy of adriamycin and paclitaxel in human osteosarcoma and non-small cell lung cancers in vivoCancer Res.64(1)31-34(2004)

Jacaric acid is a conjugated polyunsaturated fatty acid first isolated from seeds of Jacaranda plants. Structurally, it is an 18-carbon ω-6 triene isomer of γ-linolenic acid . Jacaric acid induces cell cycle arrest and apoptosis in a variety of cancer cell lines (GI50 = 1-5 μM). It increases the production of reactive oxygen species, and cytotoxicity is abolished by the antioxidant α-tocopherol, suggesting that apoptosis results from oxidative stress. Jacaric acid is metabolized in vivo to conjugated linoleic acid , which is also cytotoxic to cancer cells. Jacaric acid inhibits cyclooxygenase-1 in vitro (Ki = 1.7 μM) and, with long term feeding, decreases stearoyl-CoA desaturase expression and activity in mice.

Albanol B 是一种芳基苯并呋喃衍生物，可从桑葚中分离得到。Albanol B 具有抗阿尔茨海默病、抗菌和抗氧化活性。Albanol B 抑制癌细胞增殖，下调 CDK1表达。Albanol B 还会诱导细胞周期停滞在 G2/M 期，诱导细胞凋亡 (apoptosis)。Albanol B 诱导线粒体 ROS 产生并增加 AKT 和 ERK1/2的磷酸化水平。

TrxR-IN-3 (Compound 2c) 是TrxR 的有效抑制剂。TrxR-IN-3 对五种人类癌细胞系表现出强大的抗增殖活性，特别是对乳腺肿瘤细胞。TrxR-IN-3 增加 ROS 水平并通过调节乳腺癌细胞中细胞凋亡相关蛋白的表达导致明显的细胞凋亡。TrxR-IN-3 还通过促进 LC3-II 和 Beclin-1 的表达并减少 LC3-I 和 p62 蛋白的表达，来触发自噬体和自溶酶体的形成。

CAY10726 is an arylurea fatty acid. It decreases ATP production by 28% in MDA-MB-231 breast cancer cells when used at a concentration of 10 μM. CAY10726 decreases proliferation and initiates apoptosis in MDA-MB-231 cells via depletion of the phospholipid cardiolipin and its precursor phosphatidylglycerol from the mitochondrial membrane. In vivo, CAY10726 (2.5-40 mg kg) reduces tumor volume and increases tumor cell apoptosis in a mouse MDA-MB-231 breast cancer xenograft model in a dose-dependent manner.

(E)-2-(2-Chlorostyryl)-3,5,6-trimethylpyrazine (CSTMP) is a stilbene derivative with antioxidant and anticancer activities. It stimulates proliferation of hydrogen peroxide-damaged ECV-304 cells (EC50 = 24.9 nM). CSTMP reduces hydrogen peroxide-induced release of lactate dehydrogenase (LDH) in and increases viability of human umbilical vein endothelial cells (HUVECs) in a concentration-dependent manner via inhibition of apoptosis. It reverses hydrogen peroxide-induced release of malondialdehyde (MDA) and decreases in superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities as well as increases constitutive nitric oxide synthase (cNOS) activity and nitric oxide (NO) production in HUVECs. CSTMP also induces cell death of A549 non-small cell lung cancer (NSCLC) cells in an IRE1α-dependent manner through induction of IRE1α-TRAF2-ASK1 complex-mediated endoplasmic reticulum (ER) stress and mitochondrial apoptosis.

microRNA-21-IN-1（compound 7A）是一种高效microRNA抑制剂，对Hela和HCT-116细胞显示出抗增殖活性，IC50值分别为5.5 μM和2.8 μM，并能促进Hela细胞凋亡(apoptosis)。该化合物通过上调microRNA-21下游功能靶点（PTEN、EGR1、SLIT2）的表达，有助于抗癌研究。

UZH1 is a racemate of UZH1a and UZH1b. UZH1a is a potent and selective METTL3 inhibitor, with an IC50 of 280 nM. UZH1b (IC50=28 μM) is essentially inactive. UZH1 can be used for epitranscriptomic modulation of cellular processes. UZH1 has antitumor activity. UZH1 also can be used as a chemical probe for studying METTL3[1]. UZH1a (2.5-160 μM; 72 h) inhibits the growth of MOLM-13, HEK293T, and U2Os cells, with IC50s of 11 μM, 67 μM, and 87 μM, respectively[1].UZH1b (2.5-160 μM; 72 h) inhibits the growth of MOLM-13, HEK293T, and U2Os cells, with IC50s of 78 μM, 79 μM, and 93 μM, respectively[1].UZH1a (2.5-100 μM; 16 h) reduces m6A methylation level in mRNA from cells in a dose-dependent manner (IC50=4.6 μM), while UZH1b is less active at concentrations up to 100 μM in MOLM-13 cells[1].UZH1a (40 μM; 16 h) reduces m6A methylation level in mRNA from MOLM-13, HEK293T, and U2Os cells[1].UZH1a (20 μM; 16 h) increases apoptosis and leads to cell cycle arrest in MOLM-13 cells[1]. [1]. Moroz-Omori EV, et, al. METTL3 inhibitors for epitranscriptomic modulation of cellular processes. bioRxiv. 2020 Oct 13.

Ipivivint, a first-in-class, orally active and potent CDC-like kinase (CLK) inhibitor, inhibits CLK1 (IC50=1.4 μM), CLK2 (IC50=0.002 μM) and CLK3 (IC50=0.022 μM). Ipivivint reduces Wnt pathway signaling gene expression through inhibiting CLK activity and serine and arginine rich splicing factor (SRSF) phosphorylation and disrupting spliceosome activity. Ipivivint can be used for the research of cancer[1]. Ipivivint (SW480 cells; 0.01~10 μM; 1 hour) potently inhibits SRSF5/6 phosphorylation[1].Ipivivint (SW480 cells; 0.03 μM~3 μM; 48 hour) induced apoptosis[1]..Ipivivint (HEK-293T cells; 0.03 μM~3 μM; 1 hour) inhibits Wnt/β-catenin signaling induced by Wnt3a[1].Ipivivint (SW480 cells; 0.3~10 μM; 6 hour) increases nuclear speckle enlargement[1].Ipivivint (SW480 cells; 0.3~3μM; 24hours) significantly decreases expression of Wnt target genes (AXIN2, LEF1, MYC, and TCF7) and TCF7L2. SM08502 (SW480 cells; 0.03~3μM; 24hours) inhibits cytoplasmic or nuclear fractions protein expression. Ipivivint (NCI-N87 cells) inhibits proliferation[1].Ipivivint strongly inhibits Wnt pathway signaling activity (EC50 = 0.046 μM) in SW480 colon cancer cells[1]. Ipivivint (25 mg/kg; p.o.) potently inhibits tumor SRSF6 phosphorylation[1]. [1]. Tam BY, et al. The CLK inhibitor SM08502 induces anti-tumor activity and reduces Wnt pathway gene expression in gastrointestinal cancer models. Cancer Lett. 2020;473:186-197.

Methotrexate monohydrate is a DHhF reductase inhibitor. Methotrexate monohydrate increases T cell apoptosis, decreases T cell activation and suppresses cytokine production.

Trilexium (TRX-E-009-1)，一种第三代苯并吡喃，其结构与 TRX-E-002-1 相似。此化合物能提升 p21 蛋白的表达，并诱导细胞凋亡(apoptosis)。同时，Trilexium 亦具有解聚微管的作用，并展示出广泛的抗癌活性。

Nicotinamide-d4 is intended for use as an internal standard for the quantification of nicotinamide by GC- or LC-MS. Nicotinamide is an amide form of niacin, which is also known as vitamin B3, that can be biosynthesized in vivo or obtained through the diet. It is a precursor in the synthesis of the metabolic cofactor NAD+ and an inhibitor of sirtuin 1 (SIRT1; IC50 = <50 µM). Nicotinamide (10 µM) increases the activity of serine palmitoyltransferase (SPT) and the biosynthesis of ceramide, glucosylceramide, sphingomyelin, free fatty acids, and cholesterol in primary human keratinocytes. Nicotinamide (40 µM) induces apoptosis in SNU-398, SNU-739, and HepG2 hepatocellular carcinoma (HCC) cells, and it prevents the formation of neoplastic lesions in a diethylnitrosamine-induced mouse model of HCC. Unlike niacin, nicotinamide does not reduce plasma lipid levels or induce flushing.

PRMT5-IN-31（Compound 3m）作为一种高选择性PRMT5抑制剂，其IC50为0.31 μM。它能够通过占据PRMT5的底物位点以及与氨基酸残基形成必要相互作用来上调hnRNP E1蛋白水平。此外，PRMT5-IN-31能有效抑制A549细胞增殖，其机制涉及诱导apoptosis和阻碍细胞迁移。该化合物在人肝微粒体中表现出较高的代谢稳定性，半衰期为132.4分钟。

Antitumor agent-37 表现出有效的抗增殖和抗转移效果。Antitumor agent-37 能够诱导严重的 DNA 损伤，进而导致 γ-H2AX 和 p53 的高表达。Antitumor agent-37 可利用线粒体凋亡通路 Bcl-2/Bax/caspase3，诱导肿瘤细胞凋亡 (apoptosis)。Antitumor agent-37 可以抑制 PD-L1 的表达，提高肿瘤组织中 CD3+ 和 CD8+ T 浸润细胞，明显改善免疫反应。

T-2 Toxin (T-2 Mycotoxin) 是饲料和谷物中的各种镰刀菌种产生的真菌次生代谢产物，具有很强的生殖毒性，可诱发多种心血管毒性。T-2 Toxin 是一种抑制肽基转移酶 (60s ribosomal 亚基) 结合和蛋白质合成的抑制剂，通过ROS诱导的细胞凋亡诱导TM4细胞功能障碍，抑制 DNA 和 RNA 的合成，增加肝脏脂质过氧化物的水平。

Anticanceragent 137 (8q) 是一种高效的 PI3k 抑制剂，展现出广谱的抗肿瘤活性。它能够诱导 G2/M 阶段的细胞周期阻滞与细胞凋亡（apoptosis），并促进 PARP、caspase 3 和 caspase 7 的裂解。该化合物主要用于癌症相关的生物医学研究。

FKGK 18 is an inhibitor of group VIA (GVIA) calcium-independent phospholipase A2 (iPLA2). It inhibits GVIA iPLA2 by 99.9% at 0.091 mole fraction in a mixed micelle activity assay and is selective for GVIA iPLA2 over GIVA cPLA2 and GV sPLA2 where it shows 80.8 and 36.8% inhibition, respectively. FKGK 18 inhibits iPLA2β activity in cytosolic extracts from INS-1 cells overexpressing iPLA2β (IC50 = ~50 nM) as well as iPLA2γ activity in mouse heart membrane fractions (IC50s = ~1-3 μM). It inhibits glucose-induced increases in prostaglandin E2 production and insulin secretion in human pancreatic islets when used at a concentration of 10 μM and inhibits thapsigargin-induced apoptosis in INS-1 cells overexpressing iPLA2β in a concentration-dependent manner. FKGK 18 (20 mg/kg, 3 times per week) reduces blood glucose levels in an intraperitoneal glucose tolerance test, decreases the incidence of diabetes, and increases serum insulin levels in non-obese diabetic (NOD) mice.

Prostaglandin D2 ethanolamide (PGD2-EA) is a bioactive lipid produced by the sequential metabolism of anandamide (arachidonoyl ethanolamide) by cyclooxygenase (COX) enzymes, in particular by COX-2, and PGD synthase. The biosynthesis of PGD2-EA from anandamide can also be increased when anandamide metabolism is diminished by deletion of fatty acid amide hydrolase. PGD2-EA is inactive against recombinant prostanoid receptors, including the D prostanoid receptor. It increases the frequency of miniature inhibitory postsynaptic currents in primary cultured hippocampal neurons, an effect which is the opposite of that induced by anandamide.. PGD2-EA also induces apoptosis in colorectal carcinoma cell lines.

AlbA-DCA is a conjugate of Albiziabioside A and a dichloroacetate acid subunit that significantly enhances intracellular ROS, reduces lactic acid accumulation in the tumor microenvironment, and exhibits selectivity.

Antioxidant agent-5 (compound D-6) 是一种有效的抗氧化剂。Antioxidant agent-5 能够抑制 oxLDL 诱导的 ROS 水平升高和 NF-κB 核转位。Antioxidant agent-5 对 oxLDL (氧化型低密度脂蛋白)诱导的 VECs 细胞凋亡 (apoptosis) 及 ICAM-1 和 VCAM-1 的表达表现出抑制作用。Antioxidant agent-5 可以激活 Nrf2 HO-1 抗氧化通路，对 oxLDL 诱导的内皮损伤表现出保护活性。

SACLAC 是一种半胱天冬酶活化抑制剂，具有抗肿瘤活性，可降低AML细胞活力，抑制AML细胞增殖，增加AML细胞死亡，并诱导AML细胞凋亡，可用于研究急性髓系白血病和癌症。

Y27632 is a selective ROCK inhibitor, which inhibits ET-1-induced increases in natriuretic peptide production, cell size, protein synthesis, and myofibrillar organization. Y27632 prevents dimethylnitrosamine-induced hepatic fibrosis in rats, increases apoptosis and disrupts the actin cortical mat in embryonic avian corneal epithelium, affects initial heart myofibrillogenesis in cultured chick blastoderm, promotes the proliferation and cell cycle progression of cultured astrocyte from spinal cord.

Anticancer agent 67 是环丙沙星类似物，是一种抗癌剂，在 MCF-7 细胞中能够诱导细胞凋亡 (apoptosis) 并增加亚 G1 细胞群。

MC1742 is an inhibitor of class I histone deacetylases (HDACs; IC50s = 0.1, 0.11, 0.02, and 0.61 μM for HDAC1, -2, -3, and -8, respectively) and class IIb HDACs (IC50s = 7 and 40 nM for HDAC6 and HDAC10, respectively).1 It is selective for class I and class IIb over class IIa HDACs (IC50s = >50 μM for HDAC4, -5, -7, and -9). MC1742 reduces proliferation of HOS, MG-63, RD, A204, SK-ES-1, and A673 sarcoma cancer stem cells (CSCs). It increases levels of acetylated histone H3 and acetylated tubulin and induces apoptosis in MG-63 CSCs when used at a concentration of 2 μM. MC1742 also reactivates HIV-1 in JLAT 10.6 latently infected cells (EC50 = 350 nM).2 |1. Di Pompo, G., Salerno, M., Rotili, D., et al. Novel histone deacetylase inhibitors induce growth arrest, apoptosis, and differentiation in sarcoma cancer stem cells. J. Med. Chem. 58(9), 4073-4079 (2015).|2. Heffern, E.F.W., Ramani, R., Marshall, G., et al. Identification of isoform-selective hydroxamic acid derivatives that potently reactivate HIV from latency. J. Virus Erad. 5(2), 84-91 (2019).

AZT triphosphate TFA (3'-Azido-3'-deoxythymidine-5'-triphosphate TFA) is a active triphosphate metabolite of Zidovudine (AZT). AZT triphosphate TFA exhibits antiretroviral activity and inhibits replication of HIV. AZT triphosphate TFA also inhibits the DNA polymerase of HBV. AZT triphosphate TFA activates the mitochondria-mediated apoptosis pathway[1][2][3]. Treatment with 100 μM Zidovudine (AZT) for 48h disrupts the mitochondrial tubular network via accumulation of AZT triphosphate (AZT-TP) in H9c2 cells. AZT triphosphate accumulation causes downregulation of Opa1 and upregulation of Drp1. AZT triphosphate causes mitochondrial dysfunction, increases the production of cytotoxic reactive oxygen species (ROS), and impairs the balance of the mitochondrial quality control system in H9c2 cell model established from rat embryonic myoblasts[1]. [1]. Ryosuke Nomura, et al. Azidothymidine-triphosphate Impairs Mitochondrial Dynamics by Disrupting the Quality Control System. Redox Biol. 2017 Oct;13:407-417. [2]. Takeya Sato, et al. Engineered Human tmpk/AZT as a Novel Enzyme/Prodrug Axis for Suicide Gene Therapy. Mol Ther. 2007 May;15(5):962-70. [3]. K Y Hostetler, et al. Enhanced Oral Absorption and Antiviral Activity of 1-O-octadecyl-sn-glycero-3-phospho-acyclovir and Related Compounds in Hepatitis B Virus Infection, in Vitro. Biochem Pharmacol. 1997 Jun 15;53(12):1815-22.