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MedChemExpressModel Busulfan - 55-98-1

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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].
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Busulfan

MCE China:Busulfan

Brand:MedChemExpress (MCE)

Cat. No.HY-B0245

CAS:55-98-1

Purity:98.17%

Storage:Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month

Shipping:Room temperature in continental US; may vary elsewhere.

Description: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.

In Vitro:Busulfan (120 μM; 24 h) incited a moderate p53 activation, but strong Erk, p38, and JNK phosphorylation, in a time-dependent manner[1]. Busulfan (120 μM; 24 h) results in premature senescence in WI38 cells via the Erk and p38 MAPK pathway, reduces GSH and increases ROS production, but the production can be suppressed by NADPH oxidase[1].

In Vivo:Busulfan can be used to induce aplastic anemia models. In mice, after injections of Busulfan at doses of 16.5 mg/kg and 33 mg/kg, the measured areas under the curve are 220±34 h·nmol·mL-1 and 604±87 h·nmol·mL-1, respectively[7]. .f12{ font-size: 12px; } .fwb{ font-weight: bold; } .lh22{ line-height: 22px;; } .lh23 { line-height: 23px; } .pl13{ padding-left: 13px;; } .part { margin-top: 18px; } .mold-first-tit { width: 100%; height: 44px; line-height: 44px; background: #F9F7FB; border-bottom: 1px solid #EBE4F6; padding-left: 16px; box-sizing: border-box; margin-bottom: 17px; } .mold-second-tit:before { content:""; width: 6px; height: 6px; display: inline-block; border-radius: 50%; background: rgba(255,102,0,0.4); margin-right: 12px; position: relative; top: -3px; } .lft-border { border-left: 1px dotted #EBE4F6; padding-right: 12px; margin-left: 3px; box-sizing: border-box; padding-bottom: 12px; } /* .part .dec:last-child { border-bottom: 0; } */ .dec { margin: 10px 15px 0; padding-bottom: 10px; border-bottom: 1px dashed #EBE4F6; } .btm-border { border-left: 1px dashed #EBE4F6; } .text-bg { margin-top: 10px; background: #FFFBF1; padding: 14px; border-bottom: 0; position: relative; } .text-note-bg { margin-top: 10px; background: #FFFDF7; padding: 12px; border-bottom: 0; position: relative; } .text-note { width: 51px; height: 20px; line-height: 20px; background: #FFE2AA; text-align: center; border-radius: 0 0 8px 0; position: absolute; top: 0; left: 0; } .text-note-dec { margin-top: 15px;; } Induction of aplastic anemia model[6] Background Busulfan causes DNA damage by cross-linking DNA as well as DNA and proteins. Specific Mmodeling Methods Mice : ICR • male • 18-22 g, 6-8 weeksAdministration: 20 mg/kg busulfan+40 mg/kg cyclophosphamide• i.p. • one time per day for 12 days. Note (1) Twenty-four hours after the last intraperitoneal injection, tail vein blood was collected from eight mice randomly selected from each group for blood test.(2) the mice are sacrificed by cervical dislocation and one femur was surgically dissected. After removing epiphysis from the femur, bone marrow cells are washed off using 1 ml PBS to prepare bone marrow cell suspension. Modeling Indicators The peripheral blood cells, hemoglobin, and bone marrow nucleated cells decreased significantly.Histopathological: the proliferation of bone marrow hematopoietic tissues and cells was inhibited, and non-hematopoietic cells (fat cells) were significantly increased. Correlated Product(s): Cyclophosphamide (HY-17420) Opposite Product(s): /

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References:

[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.  [Content Brief]

[2]. Mattan Levi, et al. Treosulfan induces distinctive gonadal toxicity compared with busulfan. Oncotarget. 2018 Apr 10;9(27):19317-19327.  [Content Brief]

[3]. 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.  [Content Brief]

[4]. 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.  [Content Brief]

[5]. 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.  [Content Brief]

[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.  [Content Brief]

[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.  [Content Brief]

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