ABT-737 - CAS 852808-04-9
Not Intended for Therapeutic Use. For research use only.
Product Name:
Catalog Number:
CAS Number:
Bcl-2 Family
Chemical Structure
CAS 852808-04-9 ABT-737

Related Bcl-2 Family Products

Marinopyrrole A
(CAS: 1227962-62-0)

Marinopyrrole A, a new Mcl-1 inhibitor, could influence Mcl-1-Bim interaction and induce the degradation of Mcl-1 proteasomal and also lead to the apoptosis of ...

(CAS: 1431866-33-9)

WEHI-539, a selective BCL-XL inhibitor that can be function as a single-agent inducer of apoptosis while sparing normal cells, it leads to MOMP and apoptosis du...

(CAS: 1651890-44-6)

Pyridoclax, a pyridine derivative, has been found to be a Mcl-1 inhibitor that could induce apoptosis of cancer cells. IC50: 25 nM(Kd).

CAS 803712-79-0 Obatoclax

(CAS: 803712-79-0)

Obatoclax mesylate is the mesylate salt of obatoclax, a synthetic small-molecule inhibitor of the bcl-2 family of proteins with potential pro-apoptotic and anti...

(CAS: 1799633-27-4)

S63845, a thienopyrimidine derivative, is a potent inhibitor that specifically binds with high affinity to the BH3-binding groove of a protein of the BCL2 famil...

CAS 923564-51-6 Navitoclax

(CAS: 923564-51-6)

CAS 866541-93-7 AT-101 acetic acid

AT-101 acetic acid
(CAS: 866541-93-7)

AT101 acetic acid is orally bioavailable solvate of R-(-)-enantiomer of gossypol with potential antineoplastic activity. It is used as the treatment of non Hodg...

(CAS: 713492-66-1)

Mcl1-IN-1 is a potent Mcl-1-selective inhibitor with IC50 of 2.4 uM, relative to the related Bcl-2 family protein Bcl-xL.

CAS 1257044-40-8 ABT-199

(CAS: 1257044-40-8)

CAS 579492-81-2 Bax inhibitor peptide V5

Bax inhibitor peptide V5
(CAS: 579492-81-2)

Bax inhibitor peptide V5, a peptide inhibitor, as a pro-apoptotic member of Bcl-2 family proteins and plays an important role in mitochondria-dependent apoptosi...

(CAS: 292057-76-2)

Mcl1-IN-2, a hydroxyquinoline derivative, is an Mcl-1 inhibitor.

CAS 518303-20-3 UMI-77

(CAS: 518303-20-3)

UMI-77 is a selective Mcl-1 inhibitor with Ki of 490 nM, showing selectivity over other members of Bcl-2 family.

CAS 65673-63-4 HA14-1

(CAS: 65673-63-4)

CAS 877877-35-5 TW-37

(CAS: 877877-35-5)

TW-37, a small-molecule inhibitor of Bcl-2, inhibits cell growth and induces apoptosis in pancreatic cancer mediated through a novel pathway involving inactivat...

CAS 303-45-7 Gossypol

(CAS: 303-45-7)

Gossypol is an orally-active polyphenolic aldehyde with potential antineoplastic activity. Derived primarily from unrefined cottonseed oil, gossypol induces cel...

BDA 366
(CAS: 1821496-27-8)

BDA-366 is a BCL2-BH4 antagonist(Ki=3.3nM) which suppresses human myeloma growth. BDA-366 induces apoptosis in MM cell lines and primary MM cells by inducing BC...

CAS 331244-89-4 BAM7

(CAS: 331244-89-4)

BAM 7 is a direct and selective activator of proapoptotic Bax with EC50 of 3.3 μM.

CAS 12542-36-8 Gossypol Acetic Acid

Gossypol Acetic Acid
(CAS: 12542-36-8)

The Acetate acid salt form of gossypol which may represent a promising new anticancer agent with a novel molecular mechanism and warrants further investigation ...

(CAS: 1235034-55-5)

A-1155463, an effective and selective BCL-XL inhibitor, has been studied to have probable effect in restraining the growth of small cell lung cancer xenograft t...

(S)-Gossypol acetic acid
(CAS: 1189561-66-7)

(S)-Gossypol acetic acid, a Bcl-2 inhibitor, could effectively induce the death of Jurkat cells in which Bcl-2 or Bcl-xL is overexpressed. IC50: 18.1μM and 22.9...

Reference Reading

1.ABT-737, a BH3 mimetic, induces glutathione depletion and oxidative stress
Adrienne N. Howard, Kathleen A. Bridges, Raymond E. Meyn, Joya Chandra. Cancer Chemother Pharmacol (2009) 65:41–54
In this study, we used ABT-737 as a tool with which to further test the relationship between Bcl-2 and redox status in a human ALL cell line and in HeLa cells containing a tetracycline (tet)-repressible system for Bcl-2 expression. We find that inhibition of Bcl-2 with ABT-737 lowered intracellular GSH levels, raised intracellular ROS and caused caspase-3-dependent apoptotic DNA fragmentation. Our data suggest a mechanism where inhibition of Bcl-2 by ABT-737 results in a decrease in intracellular GSH, thereby causing caspase activation and apoptosis. We also examined the potential activity of ABT-737 in combination with ROS-inducing chemotherapeutic agents, adaphostin and etoposide, a topoisomerase-II inhibitor, in an effort to apply this knowledge towards devising therapeutic strategies incorporating Bcl-2 inhibition.
2.p53-dependent regulation of Mcl-1 contributes to synergistic cell death by ionizing radiation and the Bcl-2/Bcl-XL inhibitor ABT-737
Katrin E. Tagscherer, Anne Fassl. Apoptosis (2012) 17:187–199
To investigate the effects of a combination treatment with ABT-737 and radiotherapy, we first characterized the glioblastoma cell lines used regarding irradiation response and p53 status. LN229 and U87MG glioblastoma cell lines express wildtype p53, whereas LN18 and U251MG glioblastoma cells express mutant p53. Accordingly, IR-induced the p53 target p21 in LN229 and U87MG cells, but not in LN18 and U251MG cells (Fig. 1a, b). However, regardless of the p53 status IR resulted in a G2/M cell cycle arrest in all cell lines analyzed (Fig. 1c). Next, we investigated the effects of combined IR and ABT-737 treatment on glioblastoma cells. Irradiation followed by treatment with ABT-737 resulted in a synergistic induction of cell death in all cell lines examined (Fig. 1e). This was accompanied by a synergistic cleavage of Caspase 3 (Fig. 1d) suggesting that apoptosis at least partially contributes to the enhancement of cell death, although the involvement of other types of cell death cannot be excluded. Furthermore, we determined whether the chronological order of the single treatments affects the efficacy of the synergistic combination therapy.
3.Methylseleninic acid potentiates multiple types of cancer cells to ABT-737-induced apoptosis by targeting Mcl-1 and Bad
Shutao Yin • Yinhui Dong • Jinghua Li. Apoptosis (2012) 17:388–399
To confirm the role of Akt activation in Bad ser-136 phosphorylation and consequence of Akt activation in apoptosis induction by ABT-737, we tested effects of Akt inactivation by either pharmacological inhibitor or genetic approach on these events in MDA-MB-231 cells. As shown in Fig. 5b (left), under the condition that Akt activation was blocked by its inhibitor LY294002, ABT-737-induced Bad ser-136 phosphorylation was significantly inhibited, whereas ABT-737-induced cleavages of caspases and PARP were dramatically increased. In line with the caspases activation, inhibition of Akt by LY294002 dramatically increased ABT-737-induced apoptosis (Fig. 5b, right). These results were further verified by using siRNA approach. The data are shown in Fig. 5c, ABT-737-induced phosphorylations of Akt and Bad were significantly attenuated by knockdown of Akt, following by significant increase of caspase-3 and PARP cleavages. Taken together, the results strongly suggest that activated Akt confers cancer cells resistant to ABT-737-induced apoptosis which was associated with Bad phosphorylation.
4.Co-administration of ABT-737 and SAHA induces apoptosis, mediated by Noxa upregulation, Bax activation and mitochondrial dysfunction in PTEN-intact malignant human glioma cell lines
Kimberly A. Foster • Esther P. Jane. J Neurooncol (2014) 120:459–472
Drug resistance remains a major barrier for cancer therapeutics and multiple pathways contribute to cell death resistance in glioma. Studies have shown efficacy of the BH3-mimetic, ABT-737, in hematologic and solid malignancies. We have previously demonstrated that ABT-737 as monotherapy is ineffective in glioma cells and doses of ABT-737 above the clinically achievable range are necessary to suppress cellular proliferation. Several studies have shown that resistance to ABT-737 correlates with levels of Mcl-1 expression. We studied the pharmacologic potential of the adding an HDACI, SAHA, to ABT-737 in malignant glioma. We have previously investigated SAHA in combination therapy in malignant glioma and found induction of apoptosis when used with RTK inhibitors and proteasome inhibitors. The addition of SAHA to ABT-737 reduced cellular proliferation, promoted apoptosis and induced the expression of caspases.