Topoisomerase II ( IC50 = 36.7 μM ); Quinolone

甲磺酸加替沙星靶向 HeLa 细胞拓扑异构酶 II、大肠杆菌 NIHJ JC-2 DNA 旋转酶和金黄色葡萄球菌 MS5935 拓扑异构酶 IV，IC50 值分别为 13.8 μg/ml 和 0.109 μg/ml。和 265 μg/ml [1]。甲磺酸加替沙星的 MIC 值分别为 0.05 μg/ml 和 0.0063 μg/ml，靶向 HeLa 细胞拓扑异构酶 II、大肠杆菌 NIHJ JC-2 DNA 旋转酶和金黄色葡萄球菌 MS5935 拓扑异构酶 IV。和122微克/毫升[1]。 Gatifloxacin mesylate 对步骤一、步骤二、步骤三和步骤四突变体以及野生型菌株（MS5935、MS5952、MR5867 和 MR6009）具有抗菌活性。这些菌株的MIC值范围分别为0.05至0.10μg/ml、0.20μg/ml、1.56至3.13μg/ml、1.56至6.25μg/ml和50至200μg/ml。对于第二步和第三步突变体（MS5952、MR5867 和 MR6009）最有效的治疗是甲磺酸加替沙星，但菌株 MS5935 的第二步突变体除外 [2]。 NY12 是一种norA 转化体，可被甲磺酸加替沙星有效抑制（MIC：0.39 μg/ml）[2]。第 1 天，甲磺酸加替沙星（20-100 μM；72 小时）将胰岛素水平显着降低至 60%。第 3 天，分别 20 μM 和 100 μM 的甲磺酸加替沙星继续降低胰岛素水平。介于 44.7% 和 50.1% 之间[3]。

甲磺酸加替沙星（皮下注射；100 mg/kg；每天3次；30天）显着减少了感染巴西诺卡氏菌的小鼠足垫上的病变数量[4]。 加替沙星可降低正常和糖尿病大鼠的血清葡萄糖浓度。加替沙星导致正常和糖尿病大鼠血清肾上腺素浓度增加。 加替沙星皮下注射;100毫克/公斤;每日三次；30 d)可显著减少巴西诺卡菌小鼠脚垫损伤数[4]
100 mg/kg的加替沙星使巴西奈瑟菌HUJEG-1的血药浓度高于MIC (0.25 μg/ml) 4小时以上，血清中最高浓度为18 μg/ml（图1）。25 mg/kg的利奈唑胺也使其血药浓度高于MIC (0.12 μg/ml) 4小时以上，血清中最高浓度为50 μg/ml。考虑到这些结果，我们决定使用加替沙星100mg /kg，每日3次，皮下注射，利奈唑胺25mg /kg，每日3次。图2显示了加替沙星对病变发展的影响。这些动物显示出病变数量的减少，与利奈唑胺的效果相当。单因素方差分析结果显示，与生理盐水组相比，利奈唑胺组和加替沙星组均有统计学意义，P值为0.001。[4]

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加替沙星停药对胰岛素分泌及胰岛胰岛素含量的影响[3]
小鼠胰岛在20 μM或100 μM加替沙星中培养1天，用不含加替沙星的RPMI培养基彻底清洗，再在不含加替沙星的培养基中培养2天。加替沙星使葡萄糖诱导的胰岛素分泌大大减少，但在培养基中去除加替沙星后恢复（图5A）。加替沙星同样降低了胰岛胰岛素含量，在20 μM加替沙星组中（为对照组（0 μM加替沙星）的77%），在100 μM加替沙星组中，胰岛胰岛素含量几乎没有恢复（图5B）。由于加替沙星的存在降低了胰岛胰岛素含量，因此胰岛素分泌量以%表示，20 μM加替沙星和100 μM加替沙星培养的胰岛胰岛素释放在停药后几乎完全恢复（图5C）。

细菌酶 DNA 旋转酶和拓扑异构酶 IV 受到抗生素加替沙星的抑制，加替沙星属于第四代氟喹诺酮家族。

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酶试验。[1]
用Peng和Marians的方法测定了重组的拓扑异构酶IV的十烷癸烯化活性，并进行了少量修改。电泳分析反应，溴化乙啶染色后琼脂糖凝胶中DNA定量。用fmbioii Multi-View密度分析仪测定了着丝体DNA十烯二化单体对应的条带亮度。 DNA旋切酶的超旋切活性由Gellert等人的方法测定，稍作修改。按照拓扑异构酶IV测定方法进行分析。 拓扑异构酶II的松弛活性采用Oomori等的方法测定。 通过测定抑制50%酶反应所需的浓度（IC50）来测定每种喹诺酮类药物对II型拓扑异构酶的抑制作用。通过将HeLa细胞拓扑异构酶II的IC50除以细菌II型拓扑异构酶的IC50来确定选择性。

抗菌 与第四代氟喹诺酮抗生素家族的其他成员一样，加替沙星抑制细菌酶 DNA 旋转酶和拓扑异构酶 IV。当涉及第二步突变体（grlA gyrA；加替沙星 MIC 范围，1.56 至 3.13 microg/ml）和第三步突变体（grlA gyrA grlA；加替沙星 MIC 范围，1.56 至 6.25 microg/ml）时，加替沙星表现出活性与托舒沙星相当，比诺氟沙星、氧氟沙星、环丙沙星和司帕沙星更有效。这些结果表明，在所研究的喹诺酮类药物中，加替沙星对单突变拓扑 IV 和单突变 DNA 旋转酶具有最有效的抑制活性。对于铜绿假单胞菌感染的角膜溃疡，眼用 0.3% 加替沙星在给药频率较低时至少与环丙沙星一样有效。荧光素保留分数显示出有利于加替沙星的趋势。

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小鼠胰岛和MIN6细胞的胰岛素-2 mRNA分析[3]
50组胰岛在加或不加gatifloxacin培养3天后，使用poly(A) Pure试剂盒分离poly(A)+ rna，根据制造商说明使用SuperScript™II逆转录酶系统合成第一链cdna。TaqMan™小鼠胰岛素-2 （min -2）定量聚合酶链反应（PCR）检测在ABI PRISM™7000序列检测系统中使用正向和反向min -2特异性引物和探针。结果用min -2 mRNA与小鼠甘油醛-3-磷酸脱氢酶（GAPDH） mRNA的比值表示。 MIN6细胞在添加25 mM葡萄糖和13%胎牛血清（含或不含gatifloxacin）的Dulbecco's Minimal Essential培养基中培养3天。用TRIzol试剂制备的总RNA （10 μg）进行Northern blot分析。小鼠β-肌动蛋白mRNA进行标准化。 使用双荧光素酶报告基因检测系统（double -luciferase reporter Assay System），根据生产商说明，在转染人胰岛素启动子-荧光素酶报告基因的MIN6细胞中，用100 μM加替沙星或不加加替沙星培养3天，评估胰岛素启动子活性。相对于加替沙星未处理对照，荧光素酶活性的平均值从重复孔计算。

Animal/Disease Models: Female BALB/c mouse harboring Nocardia brasiliensis on the right hind footpad.
Doses: 100 mg/kg
Route of Administration: subcutaneous injection; 3 times a day; 30-day
Experimental Results: diminished the occurrence of injuries in mice.

Absorption, Distribution and Excretion
Well absorbed from the gastrointestinal tract after oral administration with absolute bioavailability of gatifloxacin is 96%

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Metabolism / Metabolites
Gatifloxacin undergoes limited biotransformation in humans with less than 1% of the dose excreted in the urine as ethylenediamine and methylethylenediamine metabolites
Gatifloxacin undergoes limited biotransformation in humans with less than 1% of the dose excreted in the urine as ethylenediamine and methylethylenediamine metabolites
Half Life: 7-14 hours

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Biological Half-Life
7-14 hours

Toxicity Summary
The bactericidal action of Gatifloxacin results from inhibition of the enzymes topoisomerase II (DNA gyrase) and topoisomerase IV, which are required for bacterial DNA replication, transcription, repair, and recombination.

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Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
No information is available on the clinical use of gatifloxacin during breastfeeding. Fluoroquinolones have traditionally not been used in infants because of concern about adverse effects on the infants' developing joints. However, recent studies indicate little risk. The calcium in milk might prevent absorption of the small amounts of fluoroquinolones in milk, but insufficient data exist to prove or disprove this assertion. Use of gatifloxacin is acceptable in nursing mothers with monitoring of the infant for possible effects on the gastrointestinal flora, such as diarrhea or candidiasis (thrush, diaper rash). However, it is preferable to use an alternate drug for which safety information is available.
Maternal use of an ear drop or eye drop that contains gatifloxacin presents negligible risk for the nursing infant. To substantially diminish the amount of drug that reaches the breastmilk after using eye drops, place pressure over the tear duct by the corner of the eye for 1 minute or more, then remove the excess solution with an absorbent tissue.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.

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Protein Binding
20%

[1]. Inhibitory activities of gatifloxacin (AM-1155), a newly developed fluoroquinolone, against bacterial and mammalian type II topoisomerases.Antimicrob Agents Chemother. 1998 Oct;42(10):2678-81.

[2]. Antibacterial activity of gatifloxacin (AM-1155, CG5501, BMS-206584), a newly developed fluoroquinolone, against sequentially acquired quinolone-resistant mutants and the norA transformant of Staphylococcus aureus. Antimicrob Agents Chemother. 1998 Aug;42(8):1917-22.

[3]. Gatifloxacin acutely stimulates insulin secretion and chronically suppresses insulin biosynthesis. Eur J Pharmacol. 2006 Dec 28;553(1-3):67-72.

[4]. In vivo therapeutic effect of gatifloxacin on BALB/c mice infected with Nocardia brasiliensis. Antimicrob Agents Chemother. 2008 Apr;52(4):1549-50.

Gatifloxacin Mesylate is the mesylate salt form of gatifloxacin, a synthetic 8-methoxyfluoroquinolone with antibacterial activity against a wide range of gram-negative and gram-positive microorganisms. Gatifloxacin exerts its effect through inhibition of DNA gyrase, an enzyme involved in DNA replication, transcription and repair, and inhibition of topoisomerase IV, an enzyme involved in partitioning of chromosomal DNA during bacterial cell division.

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Gatifloxacin is a monocarboxylic acid that is 4-oxo-1,4-dihydroquinoline-3-carboxylic acid which is substituted on the nitrogen by a cyclopropyl group and at positions 6, 7, and 8 by fluoro, 3-methylpiperazin-1-yl, and methoxy groups, respectively. Gatifloxacin is an antibiotic of the fourth-generation fluoroquinolone family, that like other members of that family, inhibits the bacterial topoisomerase type-II enzymes. It has a role as an antiinfective agent, an EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor and an antimicrobial agent. It is a quinolinemonocarboxylic acid, a N-arylpiperazine, an organofluorine compound, a quinolone and a quinolone antibiotic.
Gatifloxacin is an antibiotic agent and a member of the fourth-generation fluoroquinolone family. It works by inhibiting the bacterial enzymes DNA gyrase and topoisomerase IV. It was first introduced by Bristol-Myers Squibb in 1999 under the brand name Tequin® for the treatment of respiratory tract infections. Gatifloxacin is available as tablets and in various aqueous solutions for intravenous therapy. It is also available as eye drops under the brand name Zymar® marketed by Allergan. The FDA withdrew its approval for the use of non-ophthalmic drug products containing gatifloxacin due to the high prevalence of gatifloxacin-associated dysglycemia adverse event reports and the high incidence of hyperglycemic and hypoglycemic episodes in patients taking gatifloxacin compared to those on macrolide antibiotics.
Gatifloxacin anhydrous is a Quinolone Antimicrobial.
Gatifloxacin is a synthetic 8-methoxyfluoroquinolone with antibacterial activity against a wide range of gram-negative and gram-positive microorganisms. Gatifloxacin exerts its effect through inhibition of DNA gyrase, an enzyme involved in DNA replication, transcription and repair, and inhibition of topoisomerase IV, an enzyme involved in partitioning of chromosomal DNA during bacterial cell division.
Gatifloxacin is an antibiotic of the fourth-generation fluoroquinolone family, that like other members of that family, inhibits the bacterial enzymes DNA gyrase and topoisomerase IV. Bristol-Myers Squibb introduced Gatifloxacin in 1999 under the proprietary name Tequin™ for the treatment of respiratory tract infections, having licensed the medication from Kyorin Pharmaceutical Company of Japan. Allergan produces an eye-drop formulation called Zymar™. Gatifloxacin is available as tablets and in various aqueous solutions for intravenous therapy. [Wikipedia]
A fluoroquinolone antibacterial agent and DNA TOPOISOMERASE II inhibitor that is used as an ophthalmic solution for the treatment of BACTERIAL CONJUNCTIVITIS.

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Drug Indication
For the treatment of bronchitis, sinusitis, community-acquired pneumonia, and skin infections (abscesses, wounds) caused by S. pneumoniae, H. influenzae, S. aureus, M. pneumoniae, C. pneumoniae, L. pneumophila, S. pyogenes
FDA Label

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Mechanism of Action
The bactericidal action of Gatifloxacin results from inhibition of the enzymes topoisomerase II (DNA gyrase) and topoisomerase IV, which are required for bacterial DNA replication, transcription, repair, and recombination.

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Pharmacodynamics
Gatifloxacin is a synthetic broad-spectrum 8-methoxyfluoroquinolone antibacterial agent for oral or intravenous administration. is bactericidal and its mode of action depends on blocking of bacterial DNA replication by binding itself to an enzyme called DNA gyrase, which allows the untwisting required to replicate one DNA double helix into two. Notably the drug has 100 times higher affinity for bacterial DNA gyrase than for mammalian. Gatifloxacin is a broad-spectrum antibiotic that is active against both Gram-positive and Gram-negative bacteria. It should be used only to treat or prevent infections that are proven or strongly suspected to be caused by bacteria.

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We determined the inhibitory activities of gatifloxacin against Staphylococcus aureus topoisomerase IV, Escherichia coli DNA gyrase, and HeLa cell topoisomerase II and compared them with those of several quinolones. The inhibitory activities of quinolones against these type II topoisomerases significantly correlated with their antibacterial activities or cytotoxicities (correlation coefficient [r] = 0.926 for S. aureus, r = 0.972 for E. coli, and r = 0.648 for HeLa cells). Gatifloxacin possessed potent inhibitory activities against bacterial type II topoisomerases (50% inhibitory concentration [IC50] = 13.8 microg/ml for S. aureus topoisomerase IV; IC50 = 0.109 microg/ml for E. coli DNA gyrase) but the lowest activity against HeLa cell topoisomerase II (IC50 = 265 microg/ml) among the quinolones tested. There was also a significant correlation between the inhibitory activities of quinolones against S. aureus topoisomerase IV and those against E. coli DNA gyrase (r = 0.969). However, the inhibitory activity against HeLa cell topoisomerase II did not correlate with that against either bacterial enzyme. The IC50 of gatifloxacin for HeLa cell topoisomerase II was 19 and was more than 2,400 times higher than that for S. aureus topoisomerase IV and that for E. coli DNA gyrase. These ratios were higher than those for other quinolones, indicating that gatifloxacin possesses a higher selectivity for bacterial type II topoisomerases. [1]

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Alternate mutations in the grlA and gyrA genes were observed through the first- to fourth-step mutants which were obtained from four Staphylococcus aureus strains by sequential selection with several fluoroquinolones. The increases in the MICs of gatifloxacin accompanying those mutational steps suggest that primary targets of gatifloxacin in the wild type and the first-, second-, and third-step mutants are wild-type topoisomerase IV (topo IV), wild-type DNA gyrase, singly mutated topo IV, and singly mutated DNA gyrase, respectively. Gatifloxacin had activity equal to that of tosufloxacin and activity more potent than those of norfloxacin, ofloxacin, ciprofloxacin, and sparfloxacin against the second-step mutants (grlA gyrA; gatifloxacin MIC range, 1.56 to 3.13 microg/ml) and had the most potent activity against the third-step mutants (grlA gyrA grlA; gatifloxacin MIC range, 1.56 to 6.25 microg/ml), suggesting that gatifloxacin possesses the most potent inhibitory activity against singly mutated topo IV and singly mutated DNA gyrase among the quinolones tested. Moreover, gatifloxacin selected resistant mutants from wild-type and the second-step mutants at a low frequency. Gatifloxacin possessed potent activity (MIC, 0.39 microg/ml) against the NorA-overproducing strain S. aureus NY12, the norA transformant, which was slightly lower than that against the parent strain SA113. The increases in the MICs of the quinolones tested against NY12 were negatively correlated with the hydrophobicity of the quinolones (correlation coefficient, -0.93; P < 0.01). Therefore, this slight decrease in the activity of gatifloxacin is attributable to its high hydrophobicity. Those properties of gatifloxacin likely explain its good activity against quinolone-resistant clinical isolates of S. aureus harboring the grlA, gyrA, and/or norA mutations. [2]

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Gatifloxacin can cause both hypoglycemia and hyperglycemia in both diabetic and non-diabetic patients. Gatifloxacin recently has been reported to stimulate insulin secretion by inhibition of ATP-sensitive K(+) (K(ATP)) channels in pancreatic beta-cells. Gatifloxacin-induced hypoglycemia is associated with concomitant use of sulfonylureas, and usually occurs immediately after administration of the drug. We find that gatifloxacin acutely stimulates insulin secretion from mouse pancreatic islets and that glibenclamide has additive effects on gatifloxacin-induced insulin secretion. On the other hand, gatifloxacin-induced hyperglycemia often takes several days to develop. We also demonstrate that chronic gatifloxacin treatment decreases islet insulin content by inhibiting insulin biosynthesis, which process may be associated with gatifloxacin-induced hyperglycemia. Moreover, discontinuation of gatifloxacin results in improved insulin secretory response. These data clarify the differing mechanisms of gatifloxacin-induced hyper- and hypoglycemia, and suggest that blood glucose levels should be carefully monitored during gatifloxacin administration, especially in elderly patients with renal insufficiency, unrecognized diabetes, or other metabolic disorders. Because the risk of potentially life-threatening dysglycemia is increased during gatifloxacin therapy, these findings have important implications for clinical practice. [3]

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In the present work, we evaluated the effect of gatifloxacin on the evolution of experimental murine infection with Nocardia brasiliensis using linezolid as a control. Gatifloxacin was injected subcutaneously at 100 mg/kg body weight every 8 h for 4 weeks. This compound was equally as efficient as linezolid in reducing the production of lesions. [4]

C19H22N3O4F.CH4O3S

471.49974

471.147

316819-28-0

Gatifloxacin;112811-59-3;Gatifloxacin hydrochloride;121577-32-0;Gatifloxacin sesquihydrate;180200-66-2; 16819-28-0 (mesylate); 180200-66-2 (sesquihydrate); 112811-59-3; 404858-36-2 (hemihydrate); 1190043-25-4; 1189946-71-1

16040196

Typically exists as solid at room temperature

2.959

146.55

3

11

4

32

745

0

CC1NCCN(C2=C(F)C=C3C(N(C4CC4)C=C(C(O)=O)C3=O)=C2OC)C1.O=S(C)(O)=O

PMMNVFFMFJMFDB-UHFFFAOYSA-N

InChI=1S/C19H22FN3O4.CH4O3S/c1-10-8-22(6-5-21-10)16-14(20)7-12-15(18(16)27-2)23(11-3-4-11)9-13(17(12)24)19(25)26;1-5(2,3)4/h7,9-11,21H,3-6,8H2,1-2H3,(H,25,26);1H3,(H,2,3,4)

1-cyclopropyl-6-fluoro-8-methoxy-7-(3-methylpiperazin-1-yl)-4-oxoquinoline-3-carboxylic acid;methanesulfonic acid

Gatifloxacin mesylate; 316819-28-0; Gatifloxacin (mesylate); Gatifloxacin mesilate; Gatifloxacin mesylate [WHO-DD]; NZE1V6L7F9; 1-cyclopropyl-6-fluoro-8-methoxy-7-(3-methylpiperazin-1-yl)-4-oxoquinoline-3-carboxylic acid;methanesulfonic acid; 3-Quinolinecarboxylic acid, 1-cyclopropyl-6-fluoro-1,4-dihydro-8-methoxy-7-(3-methyl-1-piperazinyl)-4-oxo-, monomethanesulfonate;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

注意: 如下所列的是一些常用的体内动物实验溶解配方，主要用于溶解难溶或不溶于水的产品（水溶度<1 mg/mL）。 建议您先取少量样品进行尝试，如该配方可行，再根据实验需求增加样品量。

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注射用配方1: DMSO : Tween 80： Saline = 10 : 5 : 85 (如： 100 μL DMSO → 50 μL Tween 80 → 850 μL Saline)
*生理盐水/Saline的制备：将0.9g氯化钠/NaCl溶解在100 mL ddH ₂ O中，得到澄清溶液。
注射用配方 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL DMSO → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)
注射用配方 3: DMSO : Corn oil = 10 : 90 (如： 100 μL DMSO → 900 μL Corn oil)
示例: 以注射用配方 3 (DMSO : Corn oil = 10 : 90) 为例说明, 如果要配制 1 mL 2.5 mg/mL的工作液, 您可以取 100 μL 25 mg/mL 澄清的 DMSO 储备液，加到 900 μL Corn oil/玉米油中, 混合均匀。

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注射用配方 4: DMSO : 20% SBE-β-CD in Saline = 10 : 90 [如：100 μL DMSO → 900 μL (20% SBE-β-CD in Saline)]
*20% SBE-β-CD in Saline的制备（4°C，储存1周）：将2g SBE-β-CD (磺丁基-β-环糊精) 溶解于10mL生理盐水中，得到澄清溶液。
注射用配方 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (如： 500 μL 2-Hydroxypropyl-β-cyclodextrin (羟丙基环胡精)→ 500 μL Saline)
注射用配方 6: DMSO : PEG300 : Castor oil : Saline = 5 : 10 : 20 : 65 (如： 50 μL DMSO → 100 μL PEG300 → 200 μL Castor oil → 650 μL Saline)
注射用配方 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (如： 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
注射用配方 8: 溶解于Cremophor/Ethanol (50 : 50), 然后用生理盐水稀释。
注射用配方 9: EtOH : Corn oil = 10 : 90 (如： 100 μL EtOH → 900 μL Corn oil)
注射用配方 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL EtOH → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)

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口服配方 1: 悬浮于0.5% CMC Na (羧甲基纤维素钠)
口服配方 2: 悬浮于0.5% Carboxymethyl cellulose (羧甲基纤维素)
示例: 以口服配方 1 (悬浮于 0.5% CMC Na)为例说明, 如果要配制 100 mL 2.5 mg/mL 的工作液, 您可以先取0.5g CMC Na并将其溶解于100mL ddH2O中，得到0.5%CMC-Na澄清溶液；然后将250 mg待测化合物加到100 mL前述 0.5%CMC Na溶液中，得到悬浮液。

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口服配方 3: 溶解于 PEG400 (聚乙二醇400)
口服配方 4: 悬浮于0.2% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 5: 溶解于0.25% Tween 80 and 0.5% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 6: 做成粉末与食物混合

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注意: 以上为较为常见方法，仅供参考， InvivoChem并未独立验证这些配方的准确性。具体溶剂的选择首先应参照文献已报道溶解方法、配方或剂型，对于某些尚未有文献报道溶解方法的化合物，需通过前期实验来确定（建议先取少量样品进行尝试），包括产品的溶解情况、梯度设置、动物的耐受性等。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。