Epristeride (ONO-9302)
(Synonyms: 爱普列特; ONO-9302; SKF105657) 目录号 : GC32953
Episteride (ONO-9302) (ONO-9302) 是一种选择性、特异性和口服活性的非竞争性人类固醇 5 α-还原酶异构体 2 抑制剂。Epristeride (ONO-9302) 对 SR 同工酶 2 型具有抑制作用，Ki 值为 0.7 -2海里。 Episteride (ONO-9302) 可用于前列腺增生和痤疮的研究。
Cas No.:119169-78-7
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Epristeride is a novel 5α-reductase inhibor.
[1]. Qian LH, et al. Inhibition of regrowth of prostatic glandular cells by epristeride. Acta Pharmacol Sin. 2001 Sep;22(9):847-50.
| Cas No. | 119169-78-7 | SDF | |
| 别名 | 爱普列特; ONO-9302; SKF105657 | ||
| Canonical SMILES | C[C@@]12[C@](CC[C@@H]2C(NC(C)(C)C)=O)([H])[C@@]3([H])[C@]([C@@]4(C(C=C(C(O)=O)CC4)=CC3)C)([H])CC1 | ||
| 分子式 | C25H37NO3 | 分子量 | 399.57 |
| 溶解度 | DMSO: 100 mg/mL (250.27 mM) | 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 | 2.5027 mL | 12.5135 mL | 25.0269 mL |
| 5 mM | 0.5005 mL | 2.5027 mL | 5.0054 mL |
| 10 mM | 0.2503 mL | 1.2513 mL | 2.5027 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。
Effects of steroid 5alpha-reductase inhibitor ONO-9302 and anti-androgen allylestrenol on the prostatic growth, and plasma and prostatic hormone levels in rats
Jpn J Pharmacol 1997 Jul;74(3):243-52.PMID:9268084DOI:10.1254/jjp.74.243.
ONO-9302 [Epristeride; (-)-17beta-(tert-butylcarbamoyl)androsta-3,5-diene-3-carboxy lic acid] is a novel inhibitor of steroid 5alpha-reductase. We studied in vitro and in vivo effects of ONO-9302 on the rat prostatic tissue in comparison with those of the anti-androgen allylestrenol. ONO-9302 inhibited the rat prostatic enzyme with an IC50 value of 11 nM, whereas allylestrenol was about 80,000-fold less potent. The growth of ventral prostate, which was induced by the subcutaneous injection of testosterone propionate in the castrated rats, was significantly reduced by ONO-9302 at oral doses of 1-100 mg/kg/day. Allylestrenol showed a significant effect only at a dose of 100 mg/kg/day. In mature male rats, ONO-9302 significantly reduced the ventral prostate weight at doses of 10-100 mg/kg/day and decreased prostatic 5alpha-dihydrotestosterone (DHT) content associated with a rise in testosterone (T) content at doses of 0.1-100 mg/kg/day. Plasma hormone levels (i.e., T, DHT, luteinizing hormone (LH) and follicle stimulating hormone (FSH)) were not altered significantly. Allylestrenol significantly reduced the ventral prostate weight at doses of 10-100 mg/kg/day. However, unlike ONO-9302, allylestrenol reduced both the prostatic DHT and T contents and also lowered plasma T, DHT, LH and FSH levels at a dose of 30 mg/kg/day. These results suggest that ONO-9302 reduces the prostatic growth by inhibiting the conversion of T to DHT in the prostate without lowering blood T level unlike anti-androgen drugs.
Effects of competitive and noncompetitive 5α-reductase inhibitors on serum and intra-prostatic androgens in beagle dogs
Chin Med J (Engl) 2013 Feb;126(4):711-5.PMID:23422194doi
Background: 5α-Reductase inhibitors (5α-RI) act by inhibiting the conversion of testosterone to dihydrotestosterone (DHT), thereby preventing DHT induced benign prostatic hyperplasia. The existing 5α-RIs can be classified into two types: competitive and noncompetitive. Currently, limited evidence is available concerning the effect differences between the two types of 5α-RI on androgens. The purpose of this study was to assess the effects of competitive and noncompetitive 5α-RIs on serum and intra-prostatic androgens in beagle dogs. Methods: Twenty beagles with spontaneous benign prostatic hyperplasia were randomly allocated into two groups: Epristeride group (n = 10) in which beagles were treated with Epristeride at 1 mg/kg once a day for 3 months, and finasteride group (n = 10) in which beagles were treated with finasteride at 1 mg/kg once a day for 3 months. The levels of intra-prostatic testosterone and DHT were measured before treatment and on day one after three months medication. Serum levels of testosterone and DHT were measured at the same time points. Changes in androgen levels before and after treatment were analyzed, and comparisons were made within each treatment group and between treatment groups. Results: After 3-month treatment, serum and intra-prostatic DHT levels all decreased significantly in both the Epristeride and finasteride groups. The change of DHT in serum was significantly higher in the finasteride group (-14% and -43% in Epristeride and finasteride groups respectively, with P < 0.001); however there was no significant difference in the changes of intra-prostatic DHT between the two groups (-47% and -51% in Epristeride and finasteride groups, respectively, P = 0.304). The decreases in DHT levels were accompanied by reciprocal increases in serum and intra-prostatic testosterone levels. Changes of testosterone were significantly higher in finasteride group both in serum (20% and 42% in Epristeride and finasteride groups, respectively, P < 0.001) and in prostate tissue (18% and 29% in Epristeride and finasteride groups, respectively, P = 0.004). Conclusions: Two types of 5α-RI have similar effects in reducing DHT in prostate tissue in beagles. Competitive 5α-RI may reduce serum DHT to a greater scale, and significantly increase testosterone in beagle serum and prostate.
Epristeride SmithKline Beecham
IDrugs 1998 May;1(1):152-7.PMID:18465521doi
Epristeride is a transition-state, noncompetitive steroid 5-alpha-reductase inhibitor under development by SmithKline Beecham for the treatment of benign prostatic hyperplasia and acne. Phase III trials for prostatic hypertrophy with an oral formulation, have been initiated in the UK, the US and Japan [188478], [219166]. In healthy male volunteers, Epristeride caused a reduction in serum dihydrotestosterone levels but serum testos-terone levels remained stable. In animal studies, it showed a similar potency to finasteride for the inhibition of 5-alpha-reductase [164200]. Epristeride is licensed to Ono which has exclusive rights in Japan, South Korea and Taiwan. Recordati has co-marketing rights for Epristeride [162547], [162519]. Analysts at Yamaichi estimate that Epristeride will be launched in Japan between 1999 and 2000 and peak annual sales have been predicted to be over ten billion Yen [216018].
Inhibition of testosterone 5 alpha-reductase: evidence for tissue-specific regulation of thromboxane A2 receptors
J Pharmacol Exp Ther 1996 Dec;279(3):1386-91.PMID:8968363doi
Testosterone has been implicated as a risk factor for cardiovascular diseases and thromboxane A2 (TXA2) may be an important pathophysiologic mediator for them. Testosterone has been shown to increase TXA2 receptor density in several cell types. Testosterone is reduced at the 5 alpha position to its active metabolite, dihydrotestosterone, by 5 alpha-reductase. We determined the effects of Epristeride, a 5 alpha-reductase inhibitor, on the density of TXA2 receptors in rat aortic smooth muscle cells and human erythroleukemia cells, a megakaryocyte-like cell, in vitro, and in rat platelets and aortic membranes in vivo. In rat aortic smooth muscle cells, Epristeride significantly (P < .01, n = 5) blocked the effect of testosterone to increase TXA2 receptor density (Bmax: 44 +/- 3, 76 +/- 7, 48 +/- 4 and 46 +/- 4 fmol/mg protein, for control cells, cells treated with testosterone (200 nM), cells treated with testosterone and Epristeride (10 nM) and cells treated with Epristeride, respectively. Epristeride did not block the effect of testosterone in human erythroleukemia cells. Treatment of male rats with Epristeride for 2 weeks significantly (P < .01) decreased TXA2 receptor density in aortic membranes (41 +/- 3 for vehicle, n = 10; 27 +/- 3 fmol/mg protein for Epristeride, n = 11) but did not significantly change TXA2 receptor density in platelets. Maximum contractile responses of rat aortas to U46619, a TXA2 mimetic, were significantly (P < .001) lower in epristeride-treated rats than in vehicle-treated rats (4.2 +/- 0.1 for vehicle, n = 16, 3.0 +/- 0.2 g tension for Epristeride, n = 15). In conclusion, regulation of expression of TXA2 receptors by testosterone in cells of vascular origin, but not in platelets, appears to be via DHT.
Discovery of a novel hybrid from finasteride and Epristeride as 5α-reductase inhibitor
Bioorg Med Chem Lett 2011 Jan 1;21(1):475-8.PMID:21094046DOI:10.1016/j.bmcl.2010.10.112.
Finasteride and Epristeride both inhibit 5α-reductase with high potency via competitive and non-competitive mechanism, respectively. A new hybrid of finasteride and Epristeride was designed as a new 5α-reductase inhibitor based on combination principles in medicinal chemistry. Human 5β-reductase was chosen as a plausible surrogate of 5α-reductase type II and the results indicate that although the hybrid compound possesses the main bulk of Epristeride, its inhibitory mechanism is same as of finasteride. The hybrid turned out to be a potent 5α-reductase inhibitor in low IC(50) ranges.