ABT-737 NEW
| Price | $64 | $77 | $139 |
| Package | 5mg | 10mg | 25mg |
| Min. Order: | |
| Supply Ability: | 10g |
| Update Time: | 2024-11-14 |
Product Details
| Product Name: ABT-737 | CAS No.: 852808-04-9 |
| Purity: 99.73% | Supply Ability: 10g |
| Release date: 2024/11/14 |
Product Introduction
Bioactivity
| 名稱 | ABT-737 |
| 描述 | ABT-737 is a BH3 mimetic and an inhibitor of Bcl-2, Bcl-xL, and Bcl-w (EC50=30.3 nM/78.7 nM/197.8 nM). ABT-737 exhibits antitumor activity and anti-aging activity. |
| 細(xì)胞實(shí)驗(yàn) | Cells were seeded into 96-well plates (5 × 10^3 cells/well) and cultured for 12 h at 37 °C, as described above. Then, the medium was replaced with RPMI 1640 containing various concentrations of ATO (1, 2, 4 and 8 nM), ABT-737 (2.5, 5, 10 and 20 μM) or combinations of ATO and ABT-737, and cells were cultured for a further for 24, 48 or 72 h at 37 °C. Cells cultured in RPMI 1640 containing an equal volume of 0.01 M phosphate-buffered saline (PBS, pH 7.4; vehicle) served as controls. Cell viability was measured using Cell Counting Kit-8, according to the manufacturer's instructions. The cell proliferation rate was calculated according to the formula: experimental optical density (OD) value/control OD value × 100%. Experiments were repeated in triplicate [2]. |
| 激酶實(shí)驗(yàn) | To determine the binding affinity of GST-BCL-2 family proteins to the FITCconjugated BH3 domain of BIM, FPAs were performed as described. Briefly, 100 nM of GST-BCL-2 family fusion proteins were incubated with serial dilutions of ABT-737 in PBS for 2 min. Then, 20 nM of FITC-BIM BH3 peptide was added. Fluorescence polarization was measured using a Detection System after 10 min using the 96-well black plate. IC50s were determined [1]. |
| 動物實(shí)驗(yàn) | Mice were housed under standard conditions and had free access to water and food, under a 12-h light/12-h dark cycle in a room maintained at 18 – 22 °C and 50 – 65% humidity. SGC7901 cells (5 × 10^6) were subcutaneously inoculated into the right flank of BALB/c mice (H-2b). Tumour volume was measured using callipers and estimated according to the formula: π ? 6 × a2 × b, where a was the short axis, and b was the long axis. After 10 days, when the tumours had reached about 0.2 cm in diameter, the mice were randomly assigned to four groups (n = 8 per group), using a randomization schedule generated by the SAS software package. The groups were: control; ABT-737; ATO; ABT737 + ATO. They received, respectively: vehicle (1% DMSO, 99% 0.01 M PBS; pH 7.4); ABT-737 (50 mg/kg); ATO (2.5 mg/kg); ABT737 (50 mg/kg) + ATO (2.5 mg/kg) intraperitoneally (i.p.) every 2 days. Drugs were dissolved in the vehicle solution. To standardize the experiments, each mouse received a similar volume of solution. After 15 days, the mice were euthanized and the solid SGC-7901 tumours were harvested, fixed with 4% paraformaldehyde, frozen in optimal cutting temperature compound and stored at –80 °C [2]. |
| 體外活性 | METHODS: Neonatal rat cardiomyocyte NRCMs were incubated with Insulin (100 nM) for 48 h, and the expression levels of target proteins were detected using Western Blot. RESULTS: PE+Insulin treatment resulted in a slight decrease in relative hypertrophic protein levels compared to the PE group. TAC+GAS+Insulin induced a decrease in hypertrophy-associated proteins compared with the TAC+GAS group, and Insulin enhanced the protective effect of GAS against cardiac hypertrophy. [1] METHODS: Bovine aortic endothelial cells bAECs were incubated with Insulin (100 nM) for 10-50 min, and the expression levels of target proteins were detected using the Immunoprecipitation method. RESULTS: Insulin stimulated the phosphorylation of IRβ Tyr within 10 min, reached a maximum at 30 min, and decreased thereafter. [2] METHODS: Vascular smooth muscle cells CVSMCs were treated with Insulin (1-100 nM) for 48 h. RANKL expression was detected by qRT-PCR. RESULTS: 1 nM Insulin had no effect on RANKL mRNA expression. 5 nM Insulin stimulation resulted in a significant increase in RANKL mRNA levels, and 10 nM Insulin had the greatest effect on RANKL mRNA expression levels. At significantly supraphysiologic insulin concentrations, RANKL mRNA levels decreased slightly compared to the maximal effect of Insulin. [3] |
| 體內(nèi)活性 | METHODS: To test the antitumor activity in vivo, Insulin (0.035 mg per mouse) and anti-PD1 (0.25 mg per mouse) were intraperitoneally injected into C57BL/6 mice bearing mouse colorectal carcinoma tumor MC38 every two days for five administrations. RESULTS: anti-PD1 significantly inhibited the growth of MC38 tumors, while Insulin promoted the growth of MC38 tumors. The therapeutic effect of the combination of Insulin and anti-PD1 on MC38 tumor suppression was attenuated compared to anti-PD1 treatment alone. anti-PD1 significantly increased the number of infiltrating CD8+ T cells, whereas Insulin significantly decreased the number of tumor-infiltrating CD8+ T cells. [4] METHODS: To study virus-induced insulin-dependent diabetes mellitus (IDDM), Insulin (1 mg) was administered orally to RIP-LCMV tg mice twice a week for two months. RESULTS: Insulin treatment was effective in preventing the progression of islet infiltration to overt IDDM in pre-diabetic tg mice. Oral administration of Insulin did not affect the production of LCMV-NP-specific anti auto-cytotoxic T lymphocytes or the infiltration of lymphocytes into the pancreas. [5] |
| 存儲條件 | keep away from direct sunlight,store at low temperature | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice. |
| 溶解度 | H2O : < 1 mg/mL (insoluble or slightly soluble) Ethanol : < 1 mg/mL (insoluble or slightly soluble) DMSO : 50 mg/mL (61.47 mM) |
| 關(guān)鍵字 | Mitophagy | inhibit | mimetic | HCT116 | Apoptosis | BIM | ABT 737 | BH3 | Autophagy | AML | HL-60 | Bcl-2 Family | Mitochondrial Autophagy | BCL-2/BAX | ABT737 | Inhibitor | ABT-737 |
| 相關(guān)產(chǎn)品 | Stavudine | Xylitol | Myricetin | Sodium 4-phenylbutyrate | Hydroxychloroquine | Guanidine hydrochloride | Taurine | Curcumin | Oxyresveratrol | Paeonol | Naringin | Gefitinib |
| 相關(guān)庫 | 細(xì)胞凋亡化合物庫 | 經(jīng)典已知活性庫 | ReFRAME 相關(guān)化合物庫 | 自噬庫 | 抑制劑庫 | NO PAINS 化合物庫 | 抗衰老化合物庫 | 已知活性化合物庫 | 抗COVID-19化合物庫 | 抗癌活性化合物庫 |
Company Profile Introduction
Target Molecule Corp. (TargetMol) is a global high-tech enterprise, headquartered in Boston, MA, specializing in chemical and biological research product and service to meet the research needs of global customers.
TargetMol has evolved into one of the biggest global compound library and small molecule suppliers and a customer based on 40+ countries. TargetMol offers over 80 types of compound libraries and a wide range of high-quality research chemicals including inhibitors, activator, natural compounds, peptides, inhibitory antibodies, and novel life-science kits, for laboratory and scientific use. Besides, virtual screening service is also available for customers who would like to conduct the computer-aided drug discovery.
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United States- Since: 2011-01-07
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