br-3

CBR-3465 是结核分枝杆菌 (Mtb) II 型 NADH 脱氢酶的有效抑制剂。CBR-3465 抑制结核分枝杆菌的 MIC 值为 0.16 μM。

Dxd (OQM5SD32BQ) 是一种有效的DNA 拓扑异构酶 I 抑制剂，IC50值为 0.31 μM，用作HER2靶向ADC 的偶联药物。

Myricetin (Cannabiscetin) 属于天然类黄酮，是一种 MEK1 抑制剂。Myricetin 具有降血糖、抗氧化、保肝护肝、抗肿瘤和抗炎活性。

Lapatinib (GW572016) 是一种 ErbB2 和 EGFR 的抑制剂 (IC50=9.2 10.8 nM)，具有口服活性。Lapatinib 具有抗肿瘤活性，可以用于治疗 HER2 过表达的晚期或转移性乳腺癌。

Calcitriol (1,25-Dihydroxyvitamin D3) 是一种维他命 D 的代谢物，一种维他命 D 受体 (VDR) 的激动剂 (IC50=0.4 nM)。Calcitriol 增加肠道对钙和磷的吸收，并与甲状旁腺激素一起增加了骨吸收。

C75 是一种合成脂肪酸合酶 (FASN) 抑制剂，可抑制前列腺癌细胞 PC3 (IC50: 35 μM)。C75 增加 CPT1 活性，降低 DIO。

PK11000 是一种烷化剂，可通过共价半胱氨酸修饰来稳定野生型和突变型p53的 DNA 结合结构域。

Nordihydroguaiaretic acid (NDGA) 属于天然产物，从极叉开拉瑞阿提取，是一种脂氧合酶 (5-LOX) 抑制剂 (IC50=8 μM)。Nordihydroguaiaretic acid 具有抗氧化和清除自由基的特性。

sTGFBR3 antagonist 1 (Compound p24) 作为一种可溶性转化生长因子 β 受体 3 (sTGFBR3) 的拮抗剂,该化合物通过激活TGF-β信号通路及抑制IκBα NF-κB信号通路发挥作用.在 BV2 细胞中,sTGFBR3 antagonist 1 能有效抑制由 LPS 诱导的 NO 释放,其 IC50 值为0.52 μM.此外,该化合物还具备抗炎和神经保护的活性,并能增强血脑屏障 (BBB) 的通透性,适用于阿兹海默病的相关研究.

BR351 is a brain penetrant MMP inhibitor (IC50s: 4, 2, 11, 50 nM for MMP2, MMP8, MMP9 and MMP13).

Nortopixantrone（BBR 3438） 是一种新型9-氮杂蒽吡唑，在人前列腺癌模型中的显示出抗肿瘤活性。

Disitamab vedotin (RC-48) 是一种新开发的靶向人表皮生长因子受体2（HER2） 的抗体-活性分子偶联物 (ADC) ，由 hertuzumab 偶联单甲基 auristatin E （MMAE） 通过可切割接头组成。Disitamab vedotin 在不同HER-2表达水平胃癌细胞中显示出抗肿瘤和抗增殖活性且抑制胃癌细胞中HER-2蛋白的表达。

TCS 21311 (NIBR3049) 是一种高选择性JAK3抑制剂，IC50为 8 nM，它的选择性是 JAK1、JAK2 和 TYK2 的100倍以上，还抑制PKCα、PKCθ和GSK3β，IC50值分别为 13、68 和 3 nM。

BR351 precursor is a precursor of BR351. BR351 is a brain penetrant MMP inhibitor (IC50s: 4, 2, 11, 50 nM for MMP2, MMP8, MMP9 and MMP13).

3-Bromocytisine ((-)-3-Bromocytisine) 是一种有效的 nAChR 激动剂，对 hα4β4、hα4β2 和 hα7 的 IC50值分别为0.28、0.30 和 31.6 nM。

8-Bromo-cAMP sodium salt (8-Br-Camp sodium salt) 是一种环 AMP (cAMP) 类似物，一种 cAMP 依赖性蛋白激酶 (PKA) 的激活剂。8-Bromo-cAMP sodium salt 具有抗肿瘤活性。

Antileishmanial agent-2 是一种基于 3-Br-isoxazoline 的疟原虫抑制剂恶性疟原虫（D10 和 W2 菌株）和利什曼原虫属。 (L. infantum 和 L.tropica) 前鞭毛体，IC50 为 0.035、0.058、3.5 和 7.5 μM。

Thalidomide-piperidine-CO-piperazine-C-3-Br-Ph 属于 E3 泛素酶配体+连接子偶联物 (E3 Ligase Ligand-Linker Conjugates) 类别。该化合物主要应用于合成 PROTAC SMARCA2 degrader-28。

ERα17p (ERα 295-311)作为雌激素受体α (ER) 的钙调蛋白 (CaM) 结合表位，在钙依赖的方式下与CaM发生作用。该化合物通过Rho ROCK和PI3K Akt信号通路，调控包括MCF-7、SK-BR-3、T47D及MDA-MB-231在内的多种癌细胞迁移。同时，ERα17p对乳腺癌细胞的抑制作用包括减缓细胞增殖、诱发细胞凋亡 (apoptosis)，以及在小鼠模型中抑制肿瘤生长。

Fasnall, a fatty acid synthase (FASN) inhibitor, exhibits an IC50 of 3.71 μM against the human recombinant enzyme. It halts tritiated acetate incorporation into lipids (IC50= 5.84 μM), boosts ceramide levels, and triggers lipid droplet formation in BT474 HER2+ breast cancer cells. Demonstrating antiproliferative effects on various breast cancer cell lines, including non-tumorigenic MCF-10A and tumorigenic MCF-7, MDA-MB-468, BT474, and SK-BR-3, its efficacy is directly linked to FASN expression in vitro. In murine models of HER2+ breast cancer, particularly the MMTV-Neu model, Fasnall significantly reduces tumor volume and extends survival. Furthermore, it enhances the efficacy of carboplatin in vivo, bolstering the objective response rate of stable disease from 25% with carboplatin alone to 88% when paired with Fasnall.

Br-PEG3-OH is a PEG-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.

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)

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).

8-Br-cADPR为cADPR的高效拮抗剂,能有效减轻肾损伤并降低caspase-3与TRPM2的表达水平.