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訂貨編號(hào) | 產(chǎn)品名稱 | 規(guī)格 | 包裝 | 價(jià)格 | 操作 |
---|---|---|---|---|---|
X495677-x | 利福霉素S | 咨詢規(guī)格 | 咨詢包裝 | 咨詢價(jià)格 |
化學(xué)性質(zhì)
危險(xiǎn)屬性
質(zhì)量標(biāo)準(zhǔn)
采購詢價(jià)
熔點(diǎn) | 179-181°C (dec.) |
---|---|
比旋光度 | D20 +476° (c = 0.1 in methanol) |
沸點(diǎn) | 700.89°C (rough estimate) |
密度 | 1.2387 (rough estimate) |
折射率 | 1.6630 (estimate) |
儲(chǔ)存條件 | -20°C Freezer |
溶解度 | 苯(微量)、氯仿(微量)、甲醇(微量) |
形態(tài) | 固體 |
酸度系數(shù)(pKa) | 3.85±0.70(Predicted) |
顏色 | 橙色至深橙色 |
最大波長(λmax) | 390nm(MeOH)(lit.) |
Merck | 14,8217 |
InChIKey | BTVYFIMKUHNOBZ-ODRIEIDWSA-N |
1.疏水參數(shù)計(jì)算參考值(XlogP):4.1
2.氫鍵供體數(shù)量:4
3.氫鍵受體數(shù)量:12
4.可旋轉(zhuǎn)化學(xué)鍵數(shù)量:3
5.互變異構(gòu)體數(shù)量:339
6.拓?fù)浞肿訕O性表面積:195
7.重原子數(shù)量:50
8.表面電荷:0
9.復(fù)雜度:1480
10.同位素原子數(shù)量:0
11.確定原子立構(gòu)中心數(shù)量:9
12.不確定原子立構(gòu)中心數(shù)量:0
13.確定化學(xué)鍵立構(gòu)中心數(shù)量:3
14.不確定化學(xué)鍵立構(gòu)中心數(shù)量:0
15.共價(jià)鍵單元數(shù)量:1
RTECS號(hào) | KD1925000 |
---|---|
海關(guān)編碼 | 2941.90.1050 |
毒性 | LD50 in mice (mg/kg): 122 i.v.; 258 i.p.; 3000 orally (Sensi, 1964) |
危險(xiǎn)運(yùn)輸編碼:
危險(xiǎn)品標(biāo)志:
安全標(biāo)識(shí):
危險(xiǎn)標(biāo)識(shí):
Gram-positive bacteria
Reactive oxygen species (ROS)
The inhibition of bacterial growth by Rifamycin SV is due to the production of active species of oxygen resulting from the oxidation-reduction cycle of Rifamycin SV in the cells. The aerobic oxidation of Rifamycin SV to Rifamycin S is induced by metal ions, such as Mn 2+ , Cu 2+ , and Co 2+ . The most effective metal ion is Mn 2+ .
Rat liver sub-mitochondrial particles also generated hydroxyl radical in the presence of NADH and Rifamycin S. NADH dehydrogenase (complex I) as the major component involved in the reduction of Rifamycin S. Compared to NADPH, NADH is almost as effective (Rifamycin S) in catalyzing the interactions of these antibiotics with rat liver microsomes. Rifamycin S is shown to be readily reduced to Rifamycin SV, the corresponding hydroquinone by Fe(II). Rifamycin S forms a detectable Fe(II)-(Rifamycin S)3 complex. The Fe:ATP induced lipid peroxidation is completely inhibited by Rifamycin S. Rifamycin S can interact with rat liver microsomes to undergo redox-cycling, with the subsequent production of hydroxyl radicals when iron complexes are present.