myc in 2

MYC-IN-2 is a protein-protein inhibitor targeting the MYC protein, designed for use in cancer research.

WDR5-MYC-IN-2 是一种 WDR5-MYC 蛋白质-蛋白质相互作用 (PPI) 的抑制剂，其 IC50 为 0.59 μM。WDR5-MYC-IN-2 可用于研究 MYC 驱动型癌症及开发其他有效的 WDR5-MYC PPI 抑制剂。

c-MYC/BCL2 ligand 1 iodide 是一种联合靶向c-MYC和Bcl-2启动子区域G-四链体(G4)的配体，对c-MYCG4和Bcl-2G4的Kd值分别为0.90 μM和0.56 μM。该化合物通过结合形成G4的序列抑制c-MYC和Bcl-2基因的转录，降低其蛋白质表达。c-MYC/BCL2 ligand 1 iodide 能显著抑制MCF-7细胞增殖和迁移，并诱导细胞周期G1期阻滞与凋亡(apoptosis)。在4T1同源模型中，它有效抑制肿瘤生长且无明显毒性，适用于乳腺癌研究。

Puromycin dihydrochloride (CL13900 dihydrochloride) 属于肉桂酰胺腺苷抗生素，是一种蛋白质合成的抑制剂。Puromycin dihydrochloride 通过与 RNA 结合来抑制蛋白质合成，具有抗肿瘤和抗锥虫活性。

6-fluorinated-aristeromycin2c 具有抗病毒感染活性，对热病毒、寨卡病毒和Sars 冠状病毒具有抑制作用。

Spectinomycin dihydrochloride (Actinospectacin) 是一种能与细菌核糖体的30S 亚基结合，干扰蛋白质合成的抗生素。

Clindamycin phosphate (Clindamycin 2-dihydrogen phosphate) 是一种抗生素，抑制微生物的核糖体作用。可研究厌氧菌感染和原虫疾病。

Erythromycin 2'-propionate is a macrolide antibiotic and an esterified form of erythromycin .1It is active againstS. aureuswhen used at a concentration of 1 μg/ml. Erythromycin 2'-propionate (1 mM) inhibits protein synthesis in a cell-free assay. 1.Tardrew, P.L., Mao, J.C.H., and Kenney, D.Antibacterial activity of 2'-esters of erythromycinAppl. Microbiol.18(2)159-165(1969)

Clindamycin phosphate (Standard) 是 Clindamycin phosphate 的标准品，适用于定量分析、质量控制及生化实验等相关研究。Clindamycin phosphate (Clindamycin 2-dihydrogen phosphate) 是一种抗生素，抑制微生物的核糖体作用。可研究厌氧菌感染和原虫疾病。

Pacidamycin 2 对铜绿假单胞菌表现出抑制作用，并且对化脓性葡萄球菌和大肠杆菌等少数菌株也具有活性。

Clindamycin 2,4-diphosphate是一种用于生化反应的试剂。

Idarubicin 是一种有效的、具有口服活性的蒽环类抗白血病剂。Idarubicin 抑制拓扑异构酶 II，干扰 DNA 复制和 RNA 转录。Idarubicin 可诱导 DNA 损伤。Idarubicin 抑制 DNA 合成和 c-myc 表达。Idarubicin 还抑制细菌和酵母菌的生长。

CBP/EP300-IN-2 is an inhibitor of CBP/EP300 (IC50s: 1.07 nM and 5.96 nM for CBP/HTRF and Myc).

LZZ-02通过稳定axin 2并减少包括c-Myc和cyclin D1在内的下游蛋白水平，降解β-catenin的表达，从而抑制β-catenin的转录活性，有效缩小源自结肠细胞系的肿瘤异种移植物。

FTO-IN-13 (compound 8t) 是一种有效的FTO抑制剂，具备抗增殖和抗癌活性。该化合物能够诱导细胞凋亡 (apoptosis)，并降低Bcl-2和Caspase 3活性蛋白的表达，同时抑制MYC和CEBPA基因的表达。

HDAC3/BRD4-IN-1 (compound 26n) 是一种HDAC3/BRD4的抑制剂，其针对HDAC3的IC50为8 nM，而对HDAC1和HDAC2的IC50分别为220 nM和120 nM。HDAC3/BRD4-IN-1 展现出抗肿瘤和抗增殖作用，并通过上调Ac-H3和下调c-Myc实现。该化合物在人肝脏微粒中的半衰期为29.36分钟 (t1/2=29.36 min)。

ERK1/2 inhibitor 10 (Compound 36c) 是一种高效的ERK1和ERK2抑制剂，其IC50分别为0.11和0.08 nM。它通过抑制ERK1/2来阻碍下游底物p90RSK和c-Myc的磷酸化表达。此外，该化合物可诱导细胞凋亡 (apoptosis) 和与不完全自噬相关的细胞死亡。在携带BRAF和RAS突变的三阴性乳腺癌和结直肠癌模型中，ERK1/2 inhibitor 10显示出显著的抗肿瘤功效。

FKBP12 ligand-2 (compound d) 是一种具备高亲和力的FKBP12靶向配体。此化合物用于通过 "CellTrap" 效应选择性增强异双功能分子与BRD4的结合，从而在细胞内富集药物，形成FKBP12-配体-BRD4的三元复合物，抑制BRD4的活性。这个复合物能够抑制BRD4靶基因（如MYC）表达，导致肿瘤细胞死亡。FKBP12 ligand-2 也可以用于基于细胞内presenter蛋白水平差异的选择性癌症研究。

I3IN-002是一种小分子IGF2BP3抑制剂，IC50值在 SEM 细胞中约为 2 μM。该化合物能够干扰与m6A修饰的mRNA的相互作用，破坏目标基因（如CDK6、MYC和BCL2）的稳定性，进而抑制白血病细胞生长，诱导细胞周期停滞，并促进细胞凋亡。I3IN-002有潜力用于B细胞急性淋巴细胞白血病的研究。

PROTAC BRD4 Degrader-8 is a potent BRD4 inhibitor, with IC50s of 1.1 nM and 1.4 nM for BRD4 BD1 and BD2, respectively. PROTAC BRD4 Degrader-8 is capable of potently degrading the BRD4 protein in PC3 prostate cancer cells[1]. PROTAC BRD4 Degrader-8 (compound 8; 6 days) inhibits the proliferation of PC3 prostate cancer cells, with an IC50 of 28 nM[1].PROTAC BRD4 Degrader-8 (4 h) suppresses MYC gene transcript in MV4-11 AML cells, with an IC50 of 11 nM[1].PROTAC BRD4 Degrader-8 (4 h) potently degrades the BRD4 protein in PC3 prostate cancer cells, with an DC50 of 7.5 nM[1]. [1]. Dragovich PS, et, al. Antibody-Mediated Delivery of Chimeric BRD4 Degraders. Part 2: Improvement of In Vitro Antiproliferation Activity and In Vivo Antitumor Efficacy. J Med Chem. 2021 Mar 11;64(5):2576-2607.

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).

BRD4 Inhibitor-15 (compound 13) is a highly potent and specific inhibitor of BRD4, effectively inhibiting it with an IC50 of 18 nM. By regulating the Bcl-2/Bax proteins and activating the caspase-3 signaling pathway, BRD4 Inhibitor-15 induces apoptosis of 22RV1 cells. Additionally, it effectively down-regulates the c-Myc level in 22RV1 cells. Due to its properties, BRD4 Inhibitor-15 is a valuable compound for research related to prostate cancer [1].

P300 bromodomain-IN-1 是 p300 (EP300) bromodomain 的有效抑制剂 (IC50: 49 nM)。P300 bromodomain-IN-1 能够阻碍 c-Myc 的表达，并诱导 OPM-2 细胞的细胞周期阻滞在 G1/G0 期及诱导其凋亡 (apoptosis)。

MRK003 is a γ-secretase inhibitor exhibits promising in vitro pre-clinical activity in multiple myeloma and non-Hodgkin's lymphoma. MRK003 treatment induced caspase-dependent apoptosis and inhibited proliferation of MM and NHL cell lines and patient cells. Examination of signaling events after treatment showed time-dependent decrease in levels of the notch intracellular domain, Hes1 and c-Myc. MRK003 downregulated cyclin D1, Bcl-Xl and Xiap levels in NHL cells and p21, Bcl-2 and Bcl-Xl in MM cells. In addition, MRK003 caused an upregulation of pAkt, indicating crosstalk with the PI3K/Akt pathway.