(R)-(-)-Gossypol acetic acid

For research use only.

Catalog No.S2812 Synonyms: AT-101 acetic acid, (-)-Gossypol acetic acid, (R)-Gossypol acetic acid

14 publications

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

CAS No. 866541-93-7

(R)-(-)-Gossypol (AT-101) acetic acid, the R-(-) enantiomer of Gossypol acetic acid, binds with Bcl-2, Bcl-xL and Mcl-1 with Ki of 0.32 μM, 0.48 μM and 0.18 μM in cell-free assays; does not inhibit BIR3 domain and BID. AT-101 simultaneously triggers apoptosis and a cytoprotective type of autophagy. Phase 2.

Selleck's (R)-(-)-Gossypol acetic acid has been cited by 14 publications

5 Customer Reviews

  • (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.

Purity & Quality Control

Choose Selective Bcl-2 Inhibitors

Biological Activity

Description (R)-(-)-Gossypol (AT-101) acetic acid, the R-(-) enantiomer of Gossypol acetic acid, binds with Bcl-2, Bcl-xL and Mcl-1 with Ki of 0.32 μM, 0.48 μM and 0.18 μM in cell-free assays; does not inhibit BIR3 domain and BID. AT-101 simultaneously triggers apoptosis and a cytoprotective type of autophagy. 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)
In vitro

AT-101 inhibits a panel of different lymphoproliferative malignancies with IC50 ranged from 1.2 μM to 7.4 μM. AT-101 (10 μM) disrupts the Δψm in a concentration- and time-dependent manner in a diffuse large B-cell and in mantle cell lymphoma lines. AT-101 (1 μM or 2 μM) combined with carfilzomib (6 nM or 10 nM) induces apoptosis in HBL-2 and Granta cell lines. [2] AT-101 (20 μM for 24 hours) results in a median 72% apoptosis and down-regulation of Mcl-1 in CLL lymphocytes in both suspension culture as well as stromal coculture. Stromal cells express undetectable levels of antiapoptotic but high levels of activated ERK and AKT proteins and has low or no apoptosis with AT-101. [3] AT-101 induces apoptosis in a time- and dose-dependent fashion, with ED50 values of 1.9 mM and 2.4 mM in Jurkat T and U937 cells, respectively. AT-101 (10 μM) combined with radiation (32 Gy) induces more apoptosis than radiation alone and exceeds the sum of the effects caused by the single agent treatments. AT-101 activates SAPK/JNK in a dose- and time-dependent manner. [4] AT-101 (10 µM) induces apoptosis through activation of caspase-9, -3, and -7 in VCaP Cells. AT-101 (10 µM) decreases Bcl-2 and Mcl-1 expression in VCaP cells. [5] AT-101 (< 20 μM) is able to inhibit the growth of multiple myeloma cells despite the stimulatory growth effects provided by stromal cells in the bone marrow milieu. AT-101 (10 μM) induces apoptosis in multiple myeloma cells via the activation of caspases 3, caspases 9 and PARP. AT-101 (10 μM) promotes apoptosis in multiple myeloma cells by disrupting the Bax/Bcl-2 ratio and the mitochondrial membrane potential. [6]

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
In vivo AT-101 is still detectable in plasma with average concentrations of 0.49 μM for the 35 mg/kg group and 0.39 μM for the 200 mg/kg group in SCID beige mice bearing RL-DLBCL xenograft. AT-101 peak plasma concentration is observed after 30 minutes of administration of the drug in both the dose levels, with the 200 mg/kg group showing a plasma average concentration almost 4 times greater than the 35 mg/kg group (7.88 μM and 27.78 μM respectively) in SCID beige mice. AT-101 (25 mg/kg to 100 mg/kg, orally) indefinitely results in earlier onset of weight loss equivalent to more than 10% of the pretreatment weight and death in SCID beige mice. AT-101 (35 mg/kg, orally per day for 10 days) plus intraperitoneal cyclophosphamide (Cy) and intraperitoneal rituximab (R) show significantitumor volume control compared to any other treatment group. [2] AT-101 (15 mg/kg, p.o., 5 days/week) as a single agent in intact mice significantly reduces the development of VCaP tumor growth compared to untreated tumors at weeks 2 to 6. AT-101 in combination with surgical castration delays the onset of androgen-independent VCaP tumor growth compared to castration-only or AT-101-only groups in mice. [5]


Kinase Assay:[1]
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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
Cell Research:[2]
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  • Cell lines: RL, H9, SKI, HBL-2, Granta and JJN-3 cell lines
  • Concentrations: ~10 μM
  • Incubation Time: 72 hours
  • Method: Cells are counted and resuspended at an approximate concentration of 3×105 cells/well in a 24-well plate. AT-101 is diluted in DMSO that is maintained at a final concentration of less than 0.5%. Concentrations of AT-101 from 1 nM to 10 μM are used in most experiments. Following incubation at 37 ℃ in a 5% CO2 humidified incubator, 100 μL from each well is transferred to a 96-well opaque-walled plate; cell-Titer-Glo Reagent is added in a 1:1 ratio. Contents are mixed for 2 minutes on an orbital shaker to induce cell lysis. The plates are allowed to incubate at room temperature for 10 minutes before recording luminescence with a Synergy HT Multi-Detection Microplate Reader. In the schedule dependency experiments, serial dilutions of each drug are prepared in ratios relative to their IC50. Cells are preincubated with AT-101 for up to 72 hours, while 4-HC is added for a 24-hour period, being added at time 0, 24 hours, and 48 hours from the start of incubation. Each experiment is performed in triplicate and repeated at least twice.
    (Only for Reference)
Animal Research:[2]
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  • Animal Models: SCID beige mice bearing RL-DLBCL xenograft
  • Dosages: 100 mg/kg
  • Administration: Oral gavage
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 116 mg/mL (200.48 mM)
Water Insoluble
Ethanol ''''89 mg/mL
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+30% PEG 300+2% Tween 80+ddH2O
For best results, use promptly after mixing.

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 578.61


CAS No. 866541-93-7
Storage powder
in solvent
Synonyms AT-101 acetic acid, (-)-Gossypol acetic acid, (R)-Gossypol acetic acid
Smiles CC1=CC2=C(C(=C(C(=C2C(C)C)O)O)C=O)C(=C1C3=C(C4=C(C=C3C)C(=C(C(=C4C=O)O)O)C(C)C)O)O.CC(=O)O

In vivo Formulation Calculator (Clear solution)

Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)
Dosage mg/kg Average weight of animals g Dosing volume per animal ul Number of animals
Step 2: Enter the in vivo formulation ()
% DMSO % % Tween 80 % ddH2O

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This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )

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Clinical Trial Information

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

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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Frequently Asked Questions

  • Question 1:

    Is S2812 (-)-gossypol or another enantiomer?

  • Answer:

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

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID