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Cyclophosphamide
本产品不向个人销售，仅用作科学研究，不用于任何人体实验及非科研性质的动物实验。
Cyclophosphamide图片
CAS NO:50-18-0
包装与价格：
包装价格(元)
10mM (in 1mL DMSO)电议
50mg电议
200mg电议
500mg电议
5g电议
10g电议

产品介绍

化学性质

Physical AppearanceA solid
StorageStore at -20°C
M.Wt261.09
Cas No.50-18-0
FormulaC7H15Cl2N2O2P
Solubility≥11.85 mg/mL in H2O with gentle warming and ultrasonic; ≥13.05 mg/mL in DMSO; ≥50.8 mg/mL in EtOH
Chemical NameN,N-bis(2-chloroethyl)-2-oxo-1,3,2λ5-oxazaphosphinan-2-amine
Canonical SMILESC1CNP(=O)(OC1)N(CCCl)CCCl
运输条件蓝冰运输或根据您的需求运输。
一般建议为了使其更好的溶解，请用37℃加热试管并在超声波水浴中震动片刻。不同厂家不同批次产品溶解度各有差异，仅做参考。若实验所需浓度过大至产品溶解极限，请添加助溶剂助溶或自行调整浓度。溶液形式一般不宜长期储存，请尽快用完。

资料参考

Cyclophosphamide, an inactive prodrug, is a kind of nitrogen mustard alkylating agent. Cyclophosphamide requires enzymatic and chemical activation. As a result, nitrogen mustard is produced. It causes DNA cross-linking that accounts for its cytotoxic properties.[1]IC50of cytotoxicity in mouse embryo BALB/c 3T3 cells is 37.6 μM,[2]IC50of cytotoxicity against human HL60 cells is 8.79 μM measured by MTT assay.[3]

Cyclophosphamide attaches the alkyl group to the guanine base of DNA causing its crosslinking, strand breakage and inducing mutations.

In vitro, cyclophosphamide has a dose-dependent, bimodal effect on the immune system. Low-dose cyclophosphamide not only decreases cell number but leads to decreased functionality of regulatory T cells (TREGs). Cyclophosphamide treatment enhances apoptosis and decreases homeostatic proliferation of these cells. Expression of GITR and FoxP3, which are involved in the suppressive activity of TREGs, is down-regulated after cyclophosphamide administration.[4]In primary human hepatocyte cultures, cyclophosphamide increases CYP3A4, CYP2C8, and CYP2C9 protein levels, causing its 4-hydroxylation rate enhance.[5] In somatic cells, cyclophosphamide produces gene mutations, chromosome aberrations, micronuclei and sister chromatid exchanges in a variety of cultured cells in the presence of metabolic activation as well as sister chromatid exchanges without metabolic activation.[6]

In vivo, it has produced chromosome damage and micronuclei in rats, mice and Chinese hamsters, and gene mutations in the mouse spot test and in the transgenic lacZ construct of Muta(TM)Mouse.[6]

References:

[1] Emadi A, Jones RJ, Brodsky RA. Cyclophosphamide and cancer: golden anniversary. Nat Rev Clin Oncol. 2009 Nov; 6 (11):638-47.

[2] Moon KY, Kwon CH. N3-methyl-mafosfamide as a chemically stable, alternative prodrug of mafosfamide. Bioorg Med Chem Lett. 1998 Jul 7; 8 (13):1673-8.

[3] Patel MM, Mali MD, Patel SK. Bernthsen synthesis, antimicrobial activities and cytotoxicity of acridine derivatives. Bioorg Med Chem Lett. 2010 Nov 1; 20 (21):6324-6.

[4] Lutsiak ME, Semnani RT, De Pascalis R,et al. Inhibition of CD4(+)25+ T regulatory cell function implicated in enhanced immune response by low-dose cyclophosphamide. Blood. 2005 Apr 1; 105 (7):2862-8. Epub 2004 Dec 9.

[5] Chang TK, Yu L, Maurel P, Waxman DJ. Enhanced cyclophosphamide and ifosfamide activation in primary human hepatocyte cultures: response to cytochrome P-450 inducers and autoinduction by oxazaphosphorines. Cancer Res. 1997 May 15; 57 (10):1946-54.

[6] Anderson D, Bishop JB, Garner RC, et al. Cyclophosphamide: review of its mutagenicity for an assessment of potential germ cell risks. Mutat Res. 1995 Aug; 330 (1-2):115-81.

试验操作

Cell experiment:[1]

Cell lines

9L gliosarcoma cells retrovirally transduced withCYP2B6

Reaction Conditions

1 mM cyclophosphamide for 48 h incubation

Applications

Cyclophosphamide was shown to cause tumor cell death by stimulating apoptosis, as evidenced by the induction of plasma membrane blebbing, DNA fragmentation, and cleavage of the caspase 3 and caspase 7 substrate poly(ADP-ribose) polymerase in drug-treated cells.

Animal experiment:[2]

Animal models

Female C57BL/6 mice, 8 weeks of age

Dosage form

2 mg

Injected intraperitoneally

Applications

Low-dose cyclophosphamide not only decreased the number of regulatory T cells (TREGs), but also led to decreased functionality of TREGs. Cyclophosphamide treatment enhanced apoptosis and decreased homeostatic proliferation of these cells.

Note

The technical data provided above is for reference only.

References:

1. Schwartz PS, Waxman DJ. Cyclophosphamide induces caspase 9-dependent apoptosis in 9L tumor cells. Molecular Pharmacology, 2001, 60(6): 1268-1279.

2. Lutsiak ME, Semnani RT, De Pascalis R, et al. Inhibition of CD4(+)25+ T regulatory cell function implicated in enhanced immune response by low-dose cyclophosphamide. Blood, 2005, 105(7): 2862-2868.