Busulfan (Standard)

Busulfan (Standard) is the analytical standard of Busulfan. This product is intended for research and analytical applications. Busulfan is a potent alkylating antineoplastic agent. Busulfan causes DNA damage by cross-linking DNAs and DNA and proteins. Busulfan inhibits thioredoxin reductase. Busulfan induces apoptosis. Busulfan is an immunosuppressive and myeloablative chemotherapeutic agent[1][2][3].

55-98-1

12352100

H301, H340, H350, H360

Apoptosis; DNA Alkylator/Crosslinker; Reference Standards

Apoptosis; Cell Cycle/DNA Damage; Others

Cancer; Inflammation/Immunology

99.86

CS(=O)(OCCCCOS(C)(=O)=O)=O

C6H14O6S2

246.30

H301, H340, H350, H360

[1]Probin V, et al. Busulfan-induced senescence is dependent on ROS production upstream of the MAPK pathway. Free Radic Biol Med. 2007 Jun 15;42 (12) :1858-65. Epub 2007 Mar 31.|[2]Choi YJ, et al. Murine male germ cell apoptosis induced by busulfan treatment correlates with loss of c-kit-expression in a Fas/FasL- and p53-independent manner. FEBS Lett. 2004 Sep 24;575 (1-3) :41-51.|[3]Yoshida M, et al. Reduction of primordial follicles caused by maternal treatment with busulfan promotes endometrial adenocarcinoma development in donryu rats. J Reprod Dev. 2005 Dec;51 (6) :707-14. Epub 2005 Sep 22.|[4]Mattan Levi, et al. Treosulfan induces distinctive gonadal toxicity compared with busulfan. Oncotarget. 2018 Apr 10;9 (27) :19317-19327.|[5]Janka Reimer, et al. Antineoplastic agent busulfan regulates a network of genes related to coagulation and fibrinolysis. Eur J Clin Pharmacol. 2012 Jun;68 (6) :923-35.|[6]Chen YF, et al. The role of RIP1 and RIP3 in the development of aplastic anemia induced by cyclophosphamide and busulphan in mice. Int J Clin Exp Pathol. 2014 Dec 1;7 (12) :8411-20. |[7]Bouligand J, et al. Induction of glutathione synthesis explains pharmacodynamics of high-dose busulfan in mice and highlights putative mechanisms of drug interaction. Drug Metab Dispos. 2007 Feb;35 (2) :306-14.|[8]Probin V, et al. Busulfan-induced senescence is dependent on ROS production upstream of the MAPK pathway. Free Radic Biol Med. 2007 Jun 15;42 (12) :1858-65. Epub 2007 Mar 31.|[9]Choi YJ, et al. Murine male germ cell apoptosis induced by busulfan treatment correlates with loss of c-kit-expression in a Fas/FasL- and p53-independent manner. FEBS Lett. 2004 Sep 24;575 (1-3) :41-51.|[10]Yoshida M, et al. Reduction of primordial follicles caused by maternal treatment with busulfan promotes endometrial adenocarcinoma development in donryu rats. J Reprod Dev. 2005 Dec;51 (6) :707-14. Epub 2005 Sep 22.|[11]Mattan Levi, et al. Treosulfan induces distinctive gonadal toxicity compared with busulfan. Oncotarget. 2018 Apr 10;9 (27) :19317-19327.|[12]Janka Reimer, et al. Antineoplastic agent busulfan regulates a network of genes related to coagulation and fibrinolysis. Eur J Clin Pharmacol. 2012 Jun;68 (6) :923-35.|[13]Chen YF, et al. The role of RIP1 and RIP3 in the development of aplastic anemia induced by cyclophosphamide and busulphan in mice. Int J Clin Exp Pathol. 2014 Dec 1;7 (12) :8411-20. |[14]Bouligand J, et al. Induction of glutathione synthesis explains pharmacodynamics of high-dose busulfan in mice and highlights putative mechanisms of drug interaction. Drug Metab Dispos. 2007 Feb;35 (2) :306-14.

Blue Ice

-20°C, sealed storage, away from light and moisture