Nitromifene (CI628)
(Synonyms: 硝米芬,CI628) 目录号 : GC32445
Nitromifene (CI628) 是雌激素受体 (ER) 的拮抗剂。
Cas No.:10448-84-7
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Cell experiment: | |
References: [1]. Ruenitz PC, et al. Characterization of MCF 7 breast cancer cell growth inhibition by the antiestrogen nitromifene (CI 628) and selected metabolites. J Steroid Biochem. 1989 Sep;33(3):365-9. | |
Nitromifene is an antagonist of estrogen receptor (ER).
Nitromifene is an antagonist of estrogen receptor (ER). At 0.5 μM and 1.0 μM concentrations, Nitromifene inhibits MCF 7 cell proliferation to 70% of that in drug-free controls. At higher concentrations, Nitromifene is clearly more effective than other metabolites. Specifically bound estradiol is displaced from intact MCF 7 cells by Nitromifene. Nitromifene is an effective antagonist of the ability of calmodulin (CM) to activate cyclic nucleotide phosphodiesterase[1].
[1]. Ruenitz PC, et al. Characterization of MCF 7 breast cancer cell growth inhibition by the antiestrogen nitromifene (CI 628) and selected metabolites. J Steroid Biochem. 1989 Sep;33(3):365-9.
| Cas No. | 10448-84-7 | SDF | |
| 别名 | 硝米芬,CI628 | ||
| Canonical SMILES | O=[N+](/C(C1=CC=CC=C1)=C(C2=CC=C(OCCN3CCCC3)C=C2)/C4=CC=C(OC)C=C4)[O-] | ||
| 分子式 | C27H28N2O4 | 分子量 | 444.52 |
| 溶解度 | Soluble in DMSO | 储存条件 | Store at -20°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 | 2.2496 mL | 11.2481 mL | 22.4962 mL |
| 5 mM | 0.4499 mL | 2.2496 mL | 4.4992 mL |
| 10 mM | 0.225 mL | 1.1248 mL | 2.2496 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。
CI628 inhibits follicle-stimulating hormone (FSH)-induced increases in FSH receptors of the rat ovary: requirement of estradiol for FSH action
Endocrinology 1985 Feb;116(2):715-22.PMID:2981676DOI:10.1210/endo-116-2-715.
Although estradiol (E2) alone does not increase receptors for FSH in granulosa cells, E2 priming before administration of FSH increases numbers of FSH receptors significantly compared with FSH alone. We hypothesized that if E2 is required for FSH to increase its own receptor, blocking estrogen action should prevent FSH-induced increases in FSH receptors. Five groups of hypophysectomized rats were injected sc with: saline at 0 h; the antiestrogen CI628 (1 mg) at -6 h; human FSH (hFSH, 2 micrograms) at 0 h; CI628 at -6 h, then hFSH at 0 h; and CI628 plus E2 (2 mg) at -6 h, then FSH at 0 h. Animals were decapitated at 0, 6, 12, or 24 h, and granulosa membrane receptors for FSH, LH, and nuclear receptors for E2 were measured. LH receptor levels increased only after administration of E2 before hFSH. Treatment with hFSH for 6 h increased numbers of FSH receptors 3-fold (P less than 0.01) without any increase in numbers of E2 receptors. At 12 and 24 h, hFSH increased numbers of FSH and E2 receptors 6- and 7-fold (P less than 0.01) over controls. CI628 prevented the hFSH-induced increases in FSH receptors at 6, 12, and 24 h. Administration of E2 concomitant with CI628 before hFSH significantly reversed the inhibitory effects of CI628 on hFSH-induced increases in FSH receptors. There were no changes in affinity of FSH or E2 receptors from 0 to 24 h. To determine whether E2 was acting on the adenylate cyclase system, the ability of hFSH to increase the content of cAMP in granulosa cells in each treatment group was determined. After an iv injection of hFSH, cAMP levels were similar in CI628- and saline-treated rats but had increased 6-fold (P less than 0.01) in hFSH or CI628 plus hFSH-treated animals. Thus, blocking hFSH-induced increases in FSH and E2 receptor appeared to have no effect on FSH stimulation of cAMP. In conclusion E2 appears to be required for FSH action, perhaps by acting within granulosa cells distal to the cAMP-adenylate cyclase system.
Sexual preference and feminine and masculine sexual behavior of male rats prenatally exposed to antiandrogen or antiestrogen
Horm Behav 1995 Jun;29(2):191-206.PMID:7557922DOI:10.1006/hbeh.1995.1014.
Male rats were prenatally (Day 10-19 of pregnancy) exposed to an antiestrogen, Nitromifene citrate (CI628, 1 mg/rat), or an antiandrogen, cyproterone acetate (CA, 10 mg/rat), and in adulthood were examined for their exhibition of male-typical and female-typical behavior pattern. Treatment with CI628 abolished the capacity of the adult intact male to ejaculate, enhanced his potential to exhibit feminine sexual behavior, and decreased the intensity of the level of female-oriented behavior in a two-choice stimulus situation (estrous female vs active male). The administration of testosterone (T) did not alter these behaviors. Males exposed to CA showed low levels of lordosis behavior and normal levels of female-oriented preference. Further, they showed increased frequency of mounts and decreased number of intromissions, and only a few males ever ejaculated. Macroscopic inspection of the genital organs of the CI628-treated males revealed complete absence of the prostate. The dissections of the CA-treated males revealed a poorly developed penis and a blind-ending vagina. It was concluded that prenatal estrogen (E) is involved (1) in determining the development of mechanisms destined to mediate the display of male-typical behaviors in adulthood, (2) in suppressing the development of mechanisms of female-typical behaviors, and (3) seems to stimulate neural mechanisms influencing sexual preference behavior in the adult.
Characterization of MCF 7 breast cancer cell growth inhibition by the antiestrogen Nitromifene (CI 628) and selected metabolites
J Steroid Biochem 1989 Sep;33(3):365-9.PMID:2550704DOI:10.1016/0022-4731(89)90325-7.
Besides undergoing O-demethylation in vivo, the triarylethylene antiestrogen Nitromifene [1-(4-(2-pyrrolidinylethoxy)phenyl)-1-(4-methoxy)-phenyl-2-phenyl- 2- nitroethene, 1] undergoes biotransformation via nitroreduction, ethene bond cleavage, and pyrrolidine ring oxidation affording ketone metabolites 2 and 3 and a lactam metabolite 4. Estrogen receptor (ER) affinities of 1, 2, and 4 were, in turn, 1.7, 0.1, and 3.8% that of estradiol in MCF 7 human breast cancer cells, and these compounds inhibited by 50% the proliferation of MCF 7 cells at respective concentrations of 1.1, 5.6, and 2.0 microM. The inhibitory effect of 4 was fully reversible by estradiol, but that of 2 was only partially reversible. Also 3, which did not interact with ER, inhibited proliferation by 44% at a concentration of 10 microM. These results suggested that in contrast to 4, the effects of 2 and 3 were due in part to interaction with sites distinct from ER. Antiestrogen binding sites and calmodulin have been suggested to mediate antiproliferative effects of drugs. Interaction of ligands with the former sites has been proposed to antagonize the growth promoting effect of histamine. Although 2 and 3 had high affinities for these sites, their inhibitory effects on MCF 7 cell growth were largely unaffected by the presence of histidine, the source of intracellular histamine. Thus, the relationship between antiestrogen binding site affinity and antiproliferative effects of 2 and 3 was not clarified. In contrast, MCF 7 cell growth suppression potencies paralleled calmodulin antagonist potencies of 1 and 2 suggesting that interaction of 1 and 2 with calmodulin may contribute to their anticancer effects.
Formation of benzophenone and alpha, alpha-diarylacetophenone metabolites of the antiestrogen nitromiphene (CI628) in the presence of rat cecal contents
Life Sci 1983 Sep 12;33(11):1051-6.PMID:6412010DOI:10.1016/0024-3205(83)90660-4.
Incubation of the nonsteroidal antiestrogen nitromiphene (CI628) with rat cecal content suspension under aerobic or anaerobic conditions resulted in extensive biotransformation, yielding three metabolites, as determined by thin-layer chromatography. These metabolites were not recovered from incubation mixtures containing previously frozen suspension, and recoveries were decreased (that of nitromiphene was increased) when incubations were carried out in the presence of 2mM EDTA. Spectral and chromatographic comparison of two of the purified metabolites resulted in their structural characterization, as p-[beta(N-pyrrolidinyl)ethoxy]p'-methoxybenzophenone, and a similarly substituted alpha, alpha-diphenyl-acetophenone. These metabolites are, in turn, due formally to ethylenic bond cleavage and nitro group reduction/hydrolysis of nitromiphene.
Role of estrogen and androgen in maintaining the preovulatory follicle
Cell Tissue Res 1981;216(3):615-24.PMID:7016333DOI:10.1007/BF00238656.
The effects of Nitromifene citrate (CI 628), an antiestrogen, and Flutamide, an antiandrogen, on the ultrastructure and viability of the preovulatory follicle and granulosa cells were examined both in vivo and in vitro. In vivo administration of either antihormone induced degeneration within the granulosa cells. In some of the affected granulosa cells, the nuclear material was condensed while the cytoplasm and associated organelles were unaltered. In others, the density of the cytoplasm was reduced, the smooth endoplasmic reticulum was dilated but the nucleus remained unaltered. In vitro, either antihormone reduced granulosa-cell viability but the granulosa cells were twenty times more sensitive to CI 628 than to Flutamide. In addition, exposure to CI 628 induced nuclear condensation without affecting the cytoplasm, while Flutamide induced the deterioration of the cytoplasm without altering the nucleus. These observations suggest that: (1) both estrogen and androgens control the viability of the granulosa cells and thereby the follicle, (2) the action of estrogen and androgen is mediated through receptors within the granulosa cells since these antihormones prevent the nuclear uptake of their respective hormone, (3) the granulosa cells of preovulatory follicles appears to be more dependent on estrogen than on androgen, and (4) each steroid appears to have a specific role in maintaining the granulosa cell; estrogens control the integrity of the nucleus while androgens preserve the cytoplasmic organization of the granulosa cell.