ABT-751 hydrochloride  (Synonyms: E7010 hydrochloride)

ABT-751 (E7010) hydrochloride is a novel, highly orally bioavailable sulfonamides antimitotic compound and tubulin binder. It prevents tubulin aggregation by binding to the colchicine site on β-tubulin, leading to cell cycle arrest in G2/M phase and inducing apoptosis, thus effectively preventing cell division. ABT-751 (E7010) hydrochloride induces autophagy by inhibiting the AKT/MTOR signaling pathway. ABT-751 (E7010) hydrochloride showed significant inhibition against various types of cancer cells, including lung, gastric, colon, and breast cancer^{[1][2][3][4][5][6][7][8][9]}.

ABT-751 hydrochloride (2 μM; 4, 8, 24h) can disrupt mitosis, disrupt mitochondrial membrane potential, induce ROS generation and DNA damage in hepatocellular carcinoma-derived Hep-3B cells ^[6].
ABT-751 hydrochloride (2 μM; 4, 8, 24h) can cause DNA damage in Hep-3B cells, inhibit cell proliferation and induce G2/M cell cycle arrest ^[6].
ABT-751 hydrochloride (2 μM; 4, 8, 24h) induces autophagy in TP53-deficient Hep-3B cells by inhibiting the AKT/MTOR signaling pathway, and induces apoptosis through Caspase-dependent, exogenous, and endogenous pathways. Exogenous expression of TP53 gene further increased the autophagy and apoptosis of these cells induced by ABT-751 hydrochloride [6].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

ABT-751 hydrochloride (100 mg/kg/day, Oral gavage (p.o.), 5 days on, 5 days off x2, 21 days) has a significant inhibitory effect in neuroblastoma models and can induce significant reduction or regression of tumor volume in rhabdomyosarcoma and nephroblastoma models. ABT-751 has synergistic effect on Vincristine and Paclitaxel (HY-B0015)^[7].
ABT-751 hydrochloride (100 mg/kg/day, Oral gavage (p.o.), 5 days on, 5 days off x2) has a synergistic effect on Docetaxel (HY-B0011) in prostate, NSCLC, and breast tumor xenografts in mice. Improve the inhibitory effect on tumor^[8].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

407.87

C₁₈H₁₈ClN₃O₄S

141450-48-8

COC1=CC=C(C=C1)S(=O)(NC2=C(N=CC=C2)NC3=CC=C(C=C3)O)=O.[H]Cl

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Huang SM et al.,Tankyrase inhibition stabilizes axin and antagonizes Wnt signalling., Nature. 2009 Oct 1;461(7264):614-20.  [Content Brief]

  [2]. Elizabeth Fox et al. A Phase I Study of ABT-751, an Orally Bioavailable Tubulin Inhibitor, Administered Daily for 21 Days Every 28 Days in Pediatric Patients with Solid Tumors Clin Cancer Res February 15, 2008 14; 1111

  [3]. Aggarwal C, et al. Antiangiogenic agents in the management of non-small cell lung cancer: where do we stand now and where are we headed?,Cancer Biol Ther. 2012 Mar;13(5):247-63.  [Content Brief]

  [4]. Silver M, Rusk A, Phillips B, Beck E, Jankowski M, Philibert J, Hahn K, Hershey E, McKeegan E, Bauch J, Krivoshik A, Khanna C.,Evaluation of the oral antimitotic agent (ABT-751) in dogs with lymphoma.,J Vet Intern Med. 2012 Mar-Apr;26(2):349-54. doi: 10.1111/j.1939-1676.2012.00892.x. Epub 2012 Feb 28.  [Content Brief]

  [5]. Gaynon PS, Harned TM; for the Therapeutic Advances in Childhood LeukemiaLymphoma (TACL) Consortium.  [Content Brief]

  [6]. Yoshimatsu K, et al. Mechanism of action of E7010, an orally active sulfonamide antitumor agent: inhibition of mitosis by binding to the colchicine site of tubulin. Cancer Res. 1997;57(15):3208-3213.  [Content Brief]

  [7]. Morton CL, et al. Evaluation of ABT-751 against childhood cancer models in vivo. Invest New Drugs. 2007;25(4):285-295.  [Content Brief]

  [8]. David Frost, et al. ABT-751, an oral antimitotic, shows additive and synergistic activity with docetaxel in preclinical models. Cancer Res 1 May 2007; 67 (9_Supplement): 1426.