4-hydroperoxy Cyclophosphamide
(Synonyms: 培磷酰胺,4-OOH-CY) 目录号 : GC42401An activated analog of cyclophosphamide
Cas No.:39800-16-3
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
4-hydroperoxy Cyclophosphamide (4-OOH-CY) is the active metabolite form of the prodrug Cyclophosphamide. 4-OOH-CY crosslinks DNA and induces T cell apoptosis independent of death receptor activation, but activates mitochondrial death pathways through production of reactive oxygen species (ROS).[1] Formulations containing the prodrug Cyclophosphamide are used to treat lymphomas and autoimmune disorders.[2],[3]
4-羟基过氧化环磷（4-OOH-CY）是前药环磷酰胺的活性代谢产物。4-OOH-CY通过交联DNA和诱导T细胞凋亡来激活线粒体死亡途径，与死亡受体激活无关，但通过产生活性氧（ROS）激活线粒体死亡途径。含有前药环磷酰胺的制剂用于治疗淋巴瘤和自身免疫性疾病。
Reference:
[1]. Strauss, G., Westhoff, M.-A., Fischer-Posovszky, P., et al. 4-hydroperoxy-cyclophosphamide mediates caspase-independent T-cell apoptosis involving oxidative stress-induced nuclear relocation of mitochondrial apoptogenic factors AIF and EndoG. Cell Death Differ. 15(2), 332-343 (2008).
[2]. Ahmed, A.R., and Hombal, S.M. Cyclophosphamide (Cytoxan). A review on relevant pharmacology and clinical uses. J. Am. Acad. Dermatol. 11(6), 1115-1126 (1984).
[3]. Appel, G.B. New and future therapies for lupus nephritis. Cleve. Clin. J. Med. 79(2), 134-140 (2012).
| Cas No. | 39800-16-3 | SDF | |
| 别名 | 培磷酰胺,4-OOH-CY | ||
| 化学名 | 2-[bis(2-chloroethyl)amino]tetrahydro-2-oxido-2H-1,3,2-oxazaphosphorin-4-yl, hydroperoxide | ||
| Canonical SMILES | O=P1(N(CCCl)CCCl)OCCC(OO)N1 | ||
| 分子式 | C7H15Cl2N2O4P | 分子量 | 293.1 |
| 溶解度 | Chloroform: Slightly Soluble DMSO: Soluble | 储存条件 | -80°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.4118 mL | 17.059 mL | 34.118 mL |
| 5 mM | 0.6824 mL | 3.4118 mL | 6.8236 mL |
| 10 mM | 0.3412 mL | 1.7059 mL | 3.4118 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Combination of 4-hydroperoxy Cyclophosphamide and methotrexate inhibits IL-6/sIL-6R-induced RANKL expression in fibroblast-like synoviocytes via suppression of the JAK2/STAT3 and p38MAPK signaling pathway
Int Immunopharmacol 2018 Aug;61:45-53.PMID:29803913DOI:10.1016/j.intimp.2018.05.014.
Although conventional combination therapy is effective for most patients with rheumatoid arthritis (RA), many still do not respond to current therapies. Therefore, novel combination regimens that better target cellular processes involved in RA pathogenesis are required. Preliminary studies have demonstrated the beneficial effects of a combination of cyclophosphamide (CTX) and methotrexate (MTX) in models of RA. Using western blotting, real-time polymerase chain reaction, enzyme-linked immunosorbent assays, and immunofluorescent staining, we demonstrated that the combination of 4-hydroperoxy CTX (4-H-CTX) and MTX inhibited the expression of receptor activator of nuclear factor-κB ligand (RANKL) in fibroblast-like synoviocytes (FLS) treated with the interleukin (IL)-6/soluble IL-6 receptor (sIL-6R) complex. To elucidate the mechanisms underlying this effect, we treated RA-FLS with the JAK2/STAT3 inhibitor AG490 or p38MAPK inhibitor SB203580. The results showed that IL-6/sIL-6R-induced RANKL upregulation required phosphorylation-mediated activation of STAT3 and p38 signaling, and that 4-H-CTX and/or MTX inhibited RANKL expression in IL-6/sIL-6R-stimulated FLS by suppressing JAK2/STAT3 and p38MAPK signaling. This study demonstrated for the first time the inhibitory effects of 4-H-CTX and MTX on RANKL expression in IL-6/sIL-6R-stimulated FLS via suppression of STAT3 and p38MAPK phosphorylation. These results identify promising therapeutic agents that might have clinical applications in patients with RA who are at high risk of bone erosion or do not respond well to conventional therapy.
Ameliorative effect of recombinant human lactoferrin on the premature ovarian failure in rats after cyclophosphamide treatments
J Ovarian Res 2021 Jan 21;14(1):17.PMID:33478578DOI:10.1186/s13048-020-00763-z.
This study investigated the effect of recombinant human lactoferrin (rhLF) on the premature ovarian failure (POF) of rats. After cyclophosphamide treatments, the POF rats were divided into the following groups: normal control group (NC), low-dose group (LD), medium-dose group (MD) and high-dose group (HD) of rhLF. After drug administrations, the ovarian indexes and hormonal levels were detected. After follicle number count, the proliferation and apoptosis were analyzed with the expressions of genes related with oogenesis, reactive oxygen species (ROS) production and apoptosis detected, followed by the calculation of oxidative stress and protein expressions. After 4-hydroperoxy Cyclophosphamide (4-HC) treatments, the effect of rhLF on the proliferation, ROS production and gene expressions of primary rat granulosa cells (GCs) cultured in vitro were detected. After mating, the fertilities of POF rats were recorded. The result showed that the rhLF administrations up-regulated the ovarian index with the number of developing follicles increased and the decreases of hormonal levels conferred. The Ki-67 intensities of the MD and HD groups were up-regulated with the Tunnel intensities decreased. The rhLF treatments significantly promoted the expression of oogenesis, antioxidant and anti-apoptosis related genes. The expression of Bax and Caspase 3 were decreased with the expression of Bcl-2 up-regulated after rhLF administrations. The in vitro treatments of rhLF effectively conferred the toxicity of 4-HC on primary rat GCs. The fertility assessment showed the rhLF treatments up-regulated the offspring's' folliculogenesis, which confirmed the ameliorative role of rhLF on the POF damages via the inhibition of ROS production in GCs.