dna fragmentation

Z-FA-FMK 是一种广谱的卤代甲基酮抑制剂，可抑制冠状病毒蛋白酶3CL，Ki 为 25.7 μM。它可以不可逆地抑制半胱氨酸蛋白酶，也可以抑制效应半胱天冬酶。

5-Geranoxy-7-methoxycoumarin 是一种香豆素。它诱导细胞凋亡，具有抗癌、抗真菌和抗菌活性。

Daniquidone (Batracylin) 是一种有效的 DNA 拓扑异构酶 I 和 DNA 拓扑异构酶 II 双重抑制剂， 具有细胞毒性和抗增殖活性，可诱导 DNA 断裂，可用于研究肿瘤、免疫系统疾病和淋巴系统疾病。

Metaldehyde (Metacetaldehyde) 是一种农业中使用的软体动物杀灭剂，可在细胞中诱导 DNA 片段化。

Thymidine-5'-monophosphate disodium salt (TMP DISODIUM SALT) 是内源性代谢产物的一种。

Citric acid (Citro) 是柑橘类水果中发现的弱有机三羧酸。柠檬酸是食品添加剂和天然防腐剂。

2-Methoxyestradiol (2-ME2) 是一种口服生物可利用的雌二醇代谢物，具有抗肿瘤活性。它通过减少内皮细胞增殖和诱导内皮细胞凋亡来抑制血管生成，也可破坏微管的稳定。它可诱导半胱天冬酶活化，导致细胞周期停滞在 G2 期、DNA 断裂和细胞凋亡。

GRI977143 是 LPA2 的选择性非脂质激动剂 (EC50 = 3.3 μM)。 GRI977143 抑制半胱天冬酶 3、7、8 和 9 的激活，并减少 DNA 片段化。

ALPHA-PINENE ((-)-Alpha-Pinene) 是一种双环单萜，存在于松树和其他植物中，包括具有多种生物活性的大麻。它减少了 7 种革兰氏阳性菌、7 种革兰氏阴性菌和 8 种酵母菌株的生长，MIC 值分别为 0.75-1.29、1.05-1.59 和 0.7-1.17%。它对 C. molestus 幼虫具有杀虫活性，LC50 值范围为 47 至 49 mg L。它(100 μg ml) 可诱导细胞凋亡，增加阴离子超氧化物的产生和 DNA 片段化，并激活 B16 中的 caspase-3 F10 黑色素瘤细胞 。在 B16 F10 小鼠异种移植模型中，它（100 ml 的 10 mg ml 溶液）可将转移性肺结节的数量减少约 7 倍。它（8.6 mg L，气溶胶）还使小鼠在高架十字迷宫的张开臂​​中花费的时间增加了大约 2 倍，表明具有抗焦虑活性。

MDK83190 (Apoptosis Activator 2) 是一种细胞凋亡激活剂，可诱导 caspase-3 激活、Apaf-1 寡聚化、PARP 切割和 DNA 片段化。

N-Nitroso Atenolol 是 Atenolol 的一种衍生物。在 0.1 至 1 mM 的浓度范围内，它能诱导大鼠肝细胞的 DNA 碎片化。

9,10-Phenanthrenequinone 是一种抑制 claudin-5 CLDN5 的化合物，通过 NO 合酶 ROS 依赖的机制导致细胞凋亡。9,10-Phenanthrenequinone 也促进 Caspase 的激活和 DNA 断裂，并通过减少 CLDN5 表达以及蛋白酶体蛋白水解来引发内皮细胞屏障功能损害。

NC182 is a topo II inhibitor that shows selective and potent topo II inhibition on the induction of topo II-dependent DNA fragmentation.

4-oxo-27-TBDMS Withaferin A is a derivative of the steroidal lactone withaferin A that has anticancer activity.1 It is cytotoxic to A2780 ovarian cancer cells (IC50 = 17 μM) but not to carboplatin-resistant A2780 (A2780/CP70) cells (IC50 = >100 μM). It is selective for A2780 cells over non-cancerous ARPE19 cells (IC50 = 1,660 μM). 4-oxo-27-TBDMS Withaferin A induces DNA fragmentation in A2780 cells.References1. Perestelo, N.R., Llanos, G.G., Reyes, C.P., et al. Expanding the chemical space of withaferin A by incorporating silicon to improve its clinical potential on human ovarian carcinoma cells. J. Med. Chem. 62(9), 4571-4585 (2019). 4-oxo-27-TBDMS Withaferin A is a derivative of the steroidal lactone withaferin A that has anticancer activity.1 It is cytotoxic to A2780 ovarian cancer cells (IC50 = 17 μM) but not to carboplatin-resistant A2780 (A2780/CP70) cells (IC50 = >100 μM). It is selective for A2780 cells over non-cancerous ARPE19 cells (IC50 = 1,660 μM). 4-oxo-27-TBDMS Withaferin A induces DNA fragmentation in A2780 cells. References1. Perestelo, N.R., Llanos, G.G., Reyes, C.P., et al. Expanding the chemical space of withaferin A by incorporating silicon to improve its clinical potential on human ovarian carcinoma cells. J. Med. Chem. 62(9), 4571-4585 (2019).

C8 D-threo Ceramide is a bioactive sphingolipid and cell-permeable analog of naturally occurring ceramides. It is cytotoxic to U937 cells (IC50 = 17 μM) and induces nuclear DNA fragmentation 5- to 6-fold more potently than C8 ceramide . C8 D-threo Ceramide is a substrate for E. coli diacylglycerol kinase. It activates ceramide-activated protein kinase (CAPK) in U937 cells. C8 D-threo Ceramide also enhances V. cholerae cytolysin pore formation in liposome lipid membranes, as measured by calcein release, with a 50% release dose (RD50) value of ~5 μg ml.

C8 L-threo Ceramide is a bioactive sphingolipid and cell-permeable analog of naturally occurring ceramides. It is cytotoxic to U937 cells (IC50 = 10 μM) and, like C8 D-threo ceramide , induces nuclear DNA fragmentation 5- to 6-fold more potently than C8 L-erythro ceramide . C8 D-threo Ceramide also enhances V. cholerae cytolysin pore formation in liposome lipid membranes, as measured by calcein release, with a 50% release dose (RD50) value of ~30 μg ml.

9(E),11(E),13(E)-Octadecatrienoic acid (β-ESA) is a conjugated polyunsaturated fatty acid that is found in plant seed oils and in mixtures of conjugated linolenic acids synthesized by the alkaline isomerization of linolenic acid. It reduces growth of Caco-2 colon cancer cells in a dose-dependent and time-dependent manner. In vitro, β-ESA induces DNA fragmentation and upregulation of pro-apoptotic Bax mRNA. β-ESA decreases protein expression of the apoptosis suppression factor Bcl-2 and induces apoptosis in T24 bladder cancer cells via production of reactive oxygen species. It also inhibits bacterial fatty acid dioxygenase with a Ki value of 49 nM in vitro.

C2 Phytoceramide is a bioactive semisynthetic sphingolipid that inhibits formyl peptide-induced oxidant release (IC50 = 0.38 μM) in suspended polymorphonuclear cells. It increases COX-2 protein levels 15-fold through ERK signaling. It induces death of keratinocytes (20% viability) with an ED50 value of 30 μM, the same concentration at which 35% of cells in a TUNEL assay are apoptotic. C2 Phytoceramide also has antiproliferative effects in CHO cells, with greater than 80% cytotoxicity achieved at a concentration of 20 μM, and induces internucleosomal DNA fragmentation. In addition, it inhibits the activation of phospholipase D (PLD) mediated by muscarinic acetylcholine receptors in vitro.

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).

MMP-2 9-IN-1 (Compound 4a) 是一种有效的 MMP-2 (IC50: 56 nM) 和 MMP-9 (IC50: 38 nM) 双重抑制剂。MMP-2 9-IN-1 对肿瘤生长具有抑制作用，明显诱导癌细胞凋亡 (apoptosis)，抑制细胞迁移，并抑制细胞周期进程导致 DNA 片段化。

Dexamethasone sodium succinate is the acetate salt form of dexamethasone, which is a synthetic glucocorticoid; it combines high anti-inflammatory effects with low mineralocorticoid activity. At high doses (e.g. 40 mg), it reduces the immune response. Dexamethasone acetate (NEOFORDEX®) is indicated in adults for the treatment of symptomatic multiple myeloma in combination with other medicinal products. Dexamethasone has been shown to induce multiple myeloma cell death (apoptosis) via a down-regulation of nuclear factor-κB activity and an activation of caspase-9 through second mitochondria-derived activator of caspase (Smac; an apoptosis promoting factor) release. Prolonged exposure was required to achieve maximum levels of apoptotic markers along with increased caspase-3 activation and DNA fragmentation. Dexamethasone also down-regulated anti apoptotic genes and increased IκB-alpha protein levels. Dexamethasone apoptotic activity is enhanced by the combination with thalidomide......

Sabarubicin 是一种阿霉素双糖类似物，具有显著的抗肿瘤活性。Sabarubicin 作为一种拓扑异构酶 II 毒药比阿霉素更有效，并在较低的细胞内浓度下刺激 DNA 片段。

Mammea A BA 对克氏锥虫 (T. cruzi) 显示出有效抗性。通过诱导线粒体功能障碍、产生活性氧 (ROS)、DNA 片段化以及增加酸性液泡数量，Mammea A BA 触发细胞死亡机制，包括细胞凋亡 (apoptosis)、细胞自噬 (autophagy) 和细胞坏死，对于南美锥虫病的研究具有潜在应用价值。

Echitamine chloride 是存在于 Alstonia scholaris 中的主要单萜吲哚生物碱，具有有效的抗肿瘤活性。Echitamine chloride 会诱导 DNA 片段化和细胞凋亡 (apoptosis)。Echitamine chloride 抑制胰腺脂肪酶 (pancreatic lipase)，IC50为 10.92 µM。