药用辅料蔗糖硬脂酸酯的研究概况

蔗糖硬脂酸酯（简称＂蔗糖酯＂,结构式见图1）是由蔗糖与硬脂酸甲（乙）酯经酯交换反应合成的一类非离子表面活性剂。按单酯在总酯中的相对含量分类,主要分为蔗糖硬脂酸酯S-3、S-7、S-11和S-15。     

羧甲司坦

本品为S-(羧甲基)-半胱氨酸。按干燥品计算,含C₅H₉NO₄S应为98.0~102.0%。[性状]本品为白色结晶性粉末;无臭。本品在热水中略溶,在水中极微溶解,在乙醇或丙酮中不溶;在酸或碱溶液中易溶。     

氯美扎酮

本品为3-甲基-2-(4对氯苯基)四氢-4H-1,3-噻嗪-4-酮,1,1-二氧化物。按干燥品计算,含C₁₁H₁₂ClNO₃S应为98.0~102.0%。[性状]本品为白色结晶或结晶性粉末;有微臭。本品在丙酮与氯仿中易溶,在乙醇中微溶,在水中几乎不溶。熔点本品的熔点(中国药典1990年版二部附录15页)为112~115℃。     

环扁桃酯

本品为3,3,5-三甲基环己醇-α-苯基-α-羟基乙酸酯。按干燥品计算,含C₁₇H₂₄O₃不得少于99.0%。[性状]本品为白色或类白色的无定形粉末;有特臭,味苦。本品在乙醇或丙酮中极易溶解,在水中几乎不溶。熔点本品的熔点(中国药典1990年版二部附录15页)为50~62℃,熔距在7℃以内。     

羟甲香豆素

本品为4-甲基-7-羟基-2H-1-苯并吡喃二酮。按干燥品计算,含C₁₀H₈O₃应为98.0~102.0%。[性状]本品为白色至类白色的结晶性粉末;无臭,无味。本品在甲醇、乙醇或丙醇中略溶,在水中不溶;在氢氧化钠溶液中易溶。熔点本品的溶点(中国药典1990年版二部附录15页)为188~192℃。     

注射用盐酸甲氯芬酯

本品为盐酸甲氯芬酯的灭菌结晶或结晶性粉末。按平均装量计算,含盐酸甲氯芬酯(C₁₂H₁₆ClNO₃·HCl)应为标示量的93.0~107.0%。[性状]本品为白色结晶或结晶性粉末;略有臭、味酸苦。[鉴別]照盐酸甲氯芬酯项下的鉴别项(197页)试验,显相同的反应。     

氯噻酮

本品为3-(4-氯-3-氨磺酰基苯)-3-羟基异吲哚-1-酮。按干燥品计算,含C₁₄H₁₁ClN₂O₄S不得少于98.0%。[性状]本品为白色或类白色结晶性粉末;无臭;无味。本品在甲醇、丙酮中溶解,在乙醇中微溶,在水、乙谜、氯仿中几乎不溶。溶点本品的熔点(中国药典1990年版二部附录15页)为214~220℃,熔融时同时分解。     

单盐酸氟西泮

本品为1-[2-(二乙基氨基)乙基]-5-(2-氟苯基-7-氯-1,3-二氢-2H-1,4-苯并二氮杂-2酮酸盐。按干燥品计算,含C₂₁H₂₃C1FN₃O·HCl应为98.5~101.0%,含氯离子为8.2~8.5%。[性状]本品为白色或类白色结晶性粉末,无臭或几乎无臭。     

药用辅料蔗糖硬脂酸酯的质量标准研究

目的：修订《中华人民共和国药典》2020年版四部中蔗糖硬脂酸酯的质量标准。方法：比较国内外蔗糖硬脂酸酯质量标准,建立了HPLC法对其进行含量测定,并结合试样结果,对其分型、性状、酸值、游离蔗糖、水分、脂肪酸组成等进行增修订。结果：根据不同产品的质量和制剂中的实际应用情况,比国外药典多制订了一个分型和相应的单、二、三酯及以上多酯的限度,并对国外药典中含量测定计算公式的错误进行纠正,修订后的蔗糖硬脂酸酯质量标准已完成公示。结论：本质量标准的建立,将为蔗糖硬脂酸酯在药品中的应用提供质量保障。     

国家食品药品监督管理总局国家药品标准修订件——葡萄糖酸钠

批件号:XGB2014-019WS₁-XG-007-2014葡萄糖酸钠Putaotan gsuanna Sodium GluconateC₆H₁₁NaO₇ 218.14本品为D-葡萄糖酸钠盐。按干燥品计算,含C₆H₁₁NaO₇应为98.5%¹01.5%。【性状】本品为白色至微黄色结晶性颗粒或粉末;无臭或几乎无臭。本品在水中易溶,在无水乙醇、乙醚或三氯甲烷中几乎不溶。【鉴别】（1）取本品约0.1 g,加水5 mL溶解后,加三氯化铁试液l滴,即显深黄色。（2）取本品约0.1g,加水5 mL溶解后,加1.5%硫酸铜试液2 mL与10%氢氧化钠溶液2 mL,即显深     

Inhibition of sterol synthesis in animal cells by 15-oxygenated sterols with the unnatural cis-C-D ring junction-"5alpha,14beta-cholest-7-en-15alpha-ol-3-one and 5alpha,14beta-cholest-7-en-15beta-ol-3-one.

5α,14β-Cholest-7-en-15α-ol-3-one was prepared in 72 per cent yield by selective oxidation of the 3β-hydroxyl function of 5α,14β-cholest-7-en-3β,15α-diol by cholesterol oxidase. 5α,14β-Cholest-7-en-15β-ol-3-one was prepared in a similar manner from 5α,14β-cholest-7-en-3β,15β-diol in 66 per cent yield. The new compounds were found to inhibit sterol synthesis in mouse fibroblasts in culture. The 15α-hydroxy-3-ketosterol and the 15β-hydroxy-3-ketosterol caused a 50 per cent inhibition of the incorporation of [1?¹⁴C]acetate into digitonin-precipitable sterols at concentrations of 2.0 × 10^?6 M and 2.5 × 10^?7M, respectively, and suppressed the level of activity of 3-hydroxy-3-methylglutaryl Coenzyme A reductase activity by 50 per cent at concentrations of 3.3 × 10^?7 M and 2.5 × 10^?7 M respectively.     

Neuroscience--Fifth IBRO World Congress. 11-15 July 1999, Jerusalem, Israel

This congress, held every four years by the International Brain Research Organization (IBRO) and the World Federation of Neuroscientists, included a broad range of neuroscience presentations including many of pharmacological relevance. Delegates presented data on the pharmacological characterization and mode of action of numerous drugs at this meeting.     

Anti-inflammatory,Analgesic and Ulcerogenic Properties of S-(+)-Ibuproxam,Racemic Ibuproxam-β-cyclodextrin and S-(+)-Ibuproxam-β-cyclodextrin

The anti-inflammatory, analgesic and gastric mucosal damage-inducing activities of S-(+)-ibuproxam, and S-(+)-ibuproxam-β-cyclodextrin, new propionic acid derivatives, and racemic ibuproxam-β-cyclodextrin were investigated in three animal models and compared with those of racemic ibuproxam, racemic ibuprofen and its optical enantiomer S-(+)-ibuprofen. The anti-inflammatory activities of racemic ibuprofen, S-(+)-ibuprofen and racemic ibuproxam in carrageenan-induced paw oedema in rats were almost equipotent and slightly greater than those of S-(+)-ibuproxam and S-(+)-ibuproxam-β-cyclodextrin, and significantly greater than that of racemic ibuproxam-β-cyclodextrin. In abdominal constriction tests in mice, the analgesic effects of racemic ibuproxam, S-(+)-ibuproxam, racemic ibuproxam-β-cyclodextrin and S-(+)-ibuproxam-β-cyclodextrin were significantly less pronounced than those of racemic ibuprofen and S-(+)-ibuprofen. Ulcerogenic activity of S-(+)-ibuproxam-β-cyclodextrin in rats was found to be significantly weaker than that of racemic ibuproxam-β-cyclodextrin, racemic ibuproxam and S-(+)-ibuproxam and, most notably, weaker than those of racemic ibuprofen ans S-(+)ibuprofen. These results indicate that S-(+)-ibuproxam-β-cyclodextrin could be a novel potent anti-inflammatory and analgesic agent with a therapeutic index more favourable than that of the classical non-steroid anti-inflammatory drugs ibuprofen and ibuproxam.     

The metabolic fate of 11-bromo[15-3H]vincamine in man

During 5 days following a single oral dose of 3H-11-bromovincamine (40 mg) to two human subjects, means of 55% and 27% of the 3H dose were excreted in the urine and faeces respectively, mainly within 24 and 48 h. Mean plasma concentrations of 3H reached a peak (1900 ng equiv./ml) at 1 h after dosing and declined biphasically with half-lives of 5 h and 11 h which were similar to half-lives for urinary excretion of 3H. Parent drug and 11-bromovincaminic acid were the major dose-related components in plasma at 1.5 and 3 h. Mean plasma concentrations of 11-bromovincamine reached a peak (620 ng/ml) at 0.75 h and declined biphasically with half-lives of about 1 h and 5 h. The major urinary metabolite was 11-bromovincaminic acid (31% dose). Also present in urine were 11-bromovincamine (3%), 11-bromoapovincamine (1%) and 2 unknown metabolites (9% and 6%). Similar metabolites were detected in faecal extracts. If inadequately stored in biological samples, 11-bromovincamine could be hydrolysed to 11-bromovincaminic acid and be epimerised to 11-bromo-epivincamine.