(R)-(-)-Gossypol acetic acid

For research use only. Not for use in humans.

目录号:S2812 别名: AT-101 acetic acid, (-)-Gossypol acetic acid, (R)-Gossypol acetic acid

(R)-(-)-Gossypol acetic acid Chemical Structure

CAS No. 866541-93-7

(R)-(-)-Gossypol (AT-101) acetic acid 是醋酸棉酚的R-(-)对映体,与Bcl-2Bcl-xLMcl-1结合,无细胞试验中Ki为0.32 μM,0.48 μM 和 0.18 μM;不抑制BIR3域和BID。AT-101 可同时诱导凋亡和一种细胞保护性的自噬。Phase 2。

规格 价格 库存 购买数量  
10mM (1mL in DMSO) RMB 1562.64 现货
RMB 1202.88 现货
RMB 3834.29 现货


全国免费电话:400-668-6834   |   Email:info@selleck.cn

客户使用Selleck生产的(R)-(-)-Gossypol acetic acid发表文献14篇:


  • (B and C) assessment of antimigration capacity in each group by transwell migration assay. Abbreviations: CDDP, cisplatin; DMSO, dimethyl sulfoxide.

    Drug Des Devel Ther, 2014, 8:2517-29.. (R)-(-)-Gossypol acetic acid purchased from Selleck.

  • The cellular autophagy induced by the concentration of AT101 (5 μM) and APE1 siRNA was examined by confocal microscopy with the application of Cyto-IDr autophagy detection kit.

    Oncotarget, 2016, 7(23):34430-41. (R)-(-)-Gossypol acetic acid purchased from Selleck.

  • Effect of AT-101 (AT) on MM cell lines survival. The survival of human (MM-B1, H-Meso-1, and MM-F1) and mouse (#40a) MM cell lines were assessed by the SRB assay after 24, 48, and 72 h of treatment with DMSO or AT-101. The percentage of surviving cells treated with the compound was calculated by normalizing the OD value to that of the control cultures (DMSO). The results are expressed as the means ± SD of three independent experiments performed in triplicate (xp ≤ 0.05, ∗p ≤ 0.01, #p ≤ 0.001 compared with the cultures treated with DMSO).

    Front Pharmacol, 2018, 9:1269. (R)-(-)-Gossypol acetic acid purchased from Selleck.

  • AT-101 enhances the antimigration ability of CDDP in A549 cells exposed to A549 cell-conditioned medium. Notes: (A) The cell migration assay was conducted using Transwell® plates. A549 cells were treated with the control vehicle, 5 μM CDDP, 5 μM AT-101, or 5 μM AT-101 plus 5 μM CDDP and the supernatants were collected as the tumor conditioned medium. A549 cells were suspended in serum-free Dulbecco’s Modified Eagle’s Medium. A549 cells were seeded to the upper chambers, and the lower chambers were filled with RPMI 1640 medium containing 10% fetal bovine serum or tumor conditioned medium. After incubation for 18 hours at 37°C, cells were fixed, stained, and analyzed under inverted light microscopy (40× magnification). The number of migrated cells was counted using an inverted microscope. (B) Bar graph showing the migrating cell numbers of different treatment groups. Data are presented as the mean ± standard deviation of at least three independent experiments. **P<0.01 by one-way analysis of variance. Abbreviation: CDDP, cisplatin.

    Drug Des Devel Ther, 2015, 9:2887-910. (R)-(-)-Gossypol acetic acid purchased from Selleck.

  • AT-101 acts on Smo to inhibit Hh signaling pathway. F, BODIPYcyclopamine competition analysis. Photographs are representatives from three distinct experiments with identical results.

    Cancer Chemother Pharmacol, 2015, 76(3):461-9. . (R)-(-)-Gossypol acetic acid purchased from Selleck.




产品描述 (R)-(-)-Gossypol (AT-101) acetic acid 是醋酸棉酚的R-(-)对映体,与Bcl-2Bcl-xLMcl-1结合,无细胞试验中Ki为0.32 μM,0.48 μM 和 0.18 μM;不抑制BIR3域和BID。AT-101 可同时诱导凋亡和一种细胞保护性的自噬。Phase 2。
Mcl-1 [1]
(Cell-free assay)
Bcl-2 [1]
(Cell-free assay)
Bcl-xL [1]
(Cell-free assay)
0.18 μM(Ki) 0.32 μM(Ki) 0.48 μM(Ki)

AT-101抑制一组不同的淋巴组织增生的恶性肿瘤,处理24小时后,IC50 为1.2 μM 到 7.4 μM,处理48小时后,IC50为0.7 μM 到 3.9 μM,处理72小时后,IC50 为0.3 μM 到 1.7 μM。AT-101 (10 μM)作用于弥漫性大B细胞和套细胞淋巴瘤细胞系,破坏线粒体膜电位(Δψm),这种作用存在浓度和时间依赖性。AT-101 (1 μM or 2 μM) 与 Carfilzomib (6 nM or 10 nM) 联用作用于HBL-2 和Granta 细胞系,诱导细胞凋亡。[1]AT-101(20 μM )处理悬浮培养和基质细胞共培养的CLL淋巴细胞24小时,导致72%细胞凋亡,且下调Mcl-1。AT-101作用于表达检测不到抗凋亡水平但具有高水平激活的ERK和AKT蛋白的基质细胞,导致低的或无细胞凋亡。[2]AT-101作用于Jurkat T 和 U937 细胞,诱导凋亡,ED50值分别为1.9 mM 和 2.4 mM, 这种作用具有时间和剂量依赖性。AT-101(10 μM)与辐射(32 Gy)联合治疗与只使用辐射相比,诱导更多细胞凋亡,且治疗效果超过单剂治疗引起的效果总和。AT-101 激活SAPK/JNK,这种作用具有剂量和时间依赖性。[3] AT-101(10 µM)作用于VCaP细胞,通过激活caspase-9, -3, 和 -7而诱导凋亡。 AT-101 (10 µM) 作用于VCaP 细胞,降低Bcl-2 和 Mcl-1 表达。[4]AT-101 (< 20 μM)也抑制多发性骨髓瘤细胞生长。AT-101 (10 μM)作用于多发性骨髓瘤细胞,通过激活 caspases 3, caspases 9 和 PARP而诱导凋亡。AT-101(10 μM)作用于多发性骨髓瘤细胞,通过破坏Bax/Bcl-2比值和线粒体膜电位,而促进细胞凋亡。[5]

Methods Test Index PMID
Growth inhibition assay
Cell viability; 

PubMed: 24824755     

AT101 treated cells demonstrate a concentration- and time-dependent decrease in viability.

Western blot

PubMed: 24824755     

AT101 treated MPNST cells show a concentration-dependent increase in BNIP3 protein on western blot.

Smac / Cyt C ; 

PubMed: 22052903     

Cells were treated with 10 μm AT101 for different times and then lysed for detection of Smac and cyt c release. β-Actin was used as a protein loading control.

p53 / Cox IV ; 

PubMed: 22052903     

Cells were treated with AT101 for different times and then subjected to subcellular fraction for immunoblotting detection of p53 translocation. β-Actin and Cox IV were used as a protein loading control. WC, whole cell. 

p-AKT / AKT ; 

PubMed: 22052903     

Treated cells were lysed for detection of phosphorylated and total Akt.

APE1 / Bcl-2 / p53 / p-p53 / NF-κB ; 

PubMed: 27144437     

(D, E) The markers of BCL-2, P53, Phosphate-activated P53 (Ser15) and NF-κB were detected by western blot assay. 

24824755 22052903 27144437
体内研究 AT-101处理 携带RL-DLBCL 移植瘤的SCID米色小鼠,在血浆中仍可检测到AT-101,35 mg/kg组的平均浓度为0.49 μM,200 mg/kg组的平均浓度为0.39 μM。AT-101处理SCID米色小鼠,30分钟后观察血浆浓度峰值,200 mg/kg组的血浆平均浓度几乎比35 mg/kg组高4倍(分别为7.88 μM 和 27.78 μM)。AT-101(25 mg/kg 到 100 mg/kg)口服给药SCID米色小鼠,体重减轻的早期发病相当于使用超过10%进行预处理。AT-101(35 mg/kg,每天口服处理,持续10天)与Cyclophosphamide (Cy)(腹腔)和Rituximab (R)(腹腔)联用,与任何其他处理组相比,具有显著的肿瘤体积控制效果。[1] AT-101(15 mg/kg, 口服处理, 每周5天 )单独处理完好的小鼠,在第2到6周,与未处理组相比,显著降低VCaP肿瘤生长发生情况。AT-101与外科阉割联合处理小鼠,与只阉割处理或只使用AT-101处理组相比,延迟激素非依赖性的VCaP肿瘤生长发病情况。[4]


- 合并

Fluorescence-Polarization-Based Binding Assay:

For competitive binding experiments, Bcl-2 protein (40 nM) and FAM-Bid peptide (2.5 nM) are preincubated in the assay buffer (100 mM potassium phosphate, pH 7.5; 100 μg/mL bovine gamma globulin; 0.02% sodium azide, 5 μL of a solution in DMSO of AT101 is added to the Bcl-2/FAM-Bid solution in Dynex 96-well, black, round-bottom plates to produce a final volume of 125 μL. For each experiment, a control containing Bcl-2 and Flu-Bid peptide (equivalent to 0% inhibition), and another control containing only FAM-Bid, are included on eachassay plate. After 4 hours incubation, the polarization values in milipolarization units (mP) weremeasured at an excitation wavelength at 485 nm and an emission wavelength at 530 nm using the Ultra plate reader. IC50,the inhibitor concentration at which 50% of bound peptide is displaced, is determined from the plot using nonlinear leastsquares analysis and curve fitting performed using GraphPad Prizm 4 software. The unlabeled Bid BH3 peptide is used as the positive control. PF for Bcl-xL protein, Bak BH3 peptide labeled with 6-carboxyfluorescein succinimidyl ester (FAM-Bak) instead of the FAM-Bim to maximize the signal. It is determined that FAM-Bak has a Kd of 6 nM to Bcl-xL protein. The competitive binding assay for Bcl-xL is same as that for Bcl-2 with the following exceptions. 30 nM of Bcl-xL protein and 2.5 nM of FAM-Bak peptide in the following assay buffer: 50 mM Tris-Bis, pH 7.4 and 0.01% bovine gamma globulin. PF for Mcl-1 protein, FAM-Bid peptide and human Mcl-1 protein are used. It is determined that FAM-Bid peptide binds to human Mcl-1 protein with a Kd of 1.71 nM. The competitive binding assays for Mcl-1 are performed in the same manner as that for Bcl-2 with the following exceptions. 5 nM Mcl-1 and 1 nM Flu-Bid peptide in the following assay buffer: 25 mM Tris, pH 8.0; 150 mM NaCl and 0.05% Pluronic acid
- 合并
  • Cell lines: RL, H9, SKI, HBL-2, Granta 和 JJN-3 细胞系
  • Concentrations: 10 μM
  • Incubation Time: 72 小时
  • Method: 细胞计数,按每孔3×105个细胞的浓度再悬浮在24孔板中。AT-101在DMSO中稀释,终浓度维持在0.5%以下。在大部分实验中,AT-101 浓度为1 nM 到 10 μM。在37°C下含 5% CO2 电动培养箱中温育,每孔100 μL转移到96孔不透明板中, 按1:1的比例加入cell-Titer-Glo 试剂。在摇床上混合混合物2分钟,诱导细胞裂解。实验板在室温下温育10分钟后,使用Synergy HT多功能检测酶标仪剂量发光值。每组实验按一式三份进行,并至少重复两次。
    (Only for Reference)
- 合并
  • Animal Models: 携带RL-DLBCL 移植瘤的SCID米色小鼠
  • Dosages: 100 mg/kg
  • Administration: 口服饲喂
    (Only for Reference)

溶解度 (25°C)

体外 DMSO 116 mg/mL (200.48 mM)
Water Insoluble
Ethanol ''''89 mg/mL
体内 从左到右依次将纯溶剂加入产品,现配现用(数据来自Selleck实验检测而非文献):
2% DMSO+30% PEG 300+2% Tween 80+ddH2O

* 溶解度检测是由Selleck技术部门检测的,可能会和文献中提供的溶解度有所差异,这是由于生产工艺和批次不同产生的正常现象。请按照顺序依次加入各个纯溶剂。


分子量 578.61


CAS号 866541-93-7
储存条件 粉状
别名 AT-101 acetic acid, (-)-Gossypol acetic acid, (R)-Gossypol acetic acid

动物体内配方计算器 (澄清溶液)

给药剂量 mg/kg 动物平均体重 g 每只动物给药体积 ul 动物数量
% DMSO % % Tween 80 % ddH2O





质量 (mg) = 浓度 (mM) x 体积 (mL) x 分子量 (g/mol)


  • 质量

*在配置溶液时,请务必参考Selleck产品标签上、SDS / COA(可在Selleck的产品页面获得)批次特异的分子量使用本工具。




开始浓度 x 开始体积 = 最终浓度 x 最终体积


稀释公式一般简略地表示为: C1V1 = C2V2 ( 输入 输出 )

  • C1

在配置溶液时,请务必参考Selleck产品标签上、SDS / COA(可在Selleck的产品页面获得)批次特异的分子量使用本工具。.


  • 连续稀释

  • 计算结果

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):




注:化学分子式大小写敏感。C10H16N2O2 c10h16n2o2


质量 浓度 体积 分子量


NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT00934076 Withdrawn Drug: Tarceva plus AT-101 Carcinoma Non Small Cell Lung University of Alabama at Birmingham|Ascenta Therapeutics February 2010 Phase 1
NCT00561197 Terminated Drug: AT-101 Locally Advanced Esophageal or GE Junction Cancer Ascenta Therapeutics August 2007 Phase 1|Phase 2
NCT00286793 Completed Drug: AT-101 Prostate Cancer Ascenta Therapeutics February 2006 Phase 1|Phase 2





  • * 必填项


  • 问题 1:

    Is S2812 (-)-gossypol or another enantiomer?

  • 回答:

    S2812 AT101 is R-(–)-gossypolacetic acid.


Bcl-2 Signaling Pathway Map

Bcl-2 Inhibitors with Unique Features


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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID