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| 10 mM * 1 mL in DMSO |
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| 10 mM * 1 mL in DMSO |
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| 靶点 |
CysLT1/cysteinyl leukotriene receptor 1
Montelukast (5 μM; 1 h) prevents cell damage caused by APAP (acetaminophen) (HY-66005)[1]. Montelukast (0.01-10 μM; 30 min) attenuates the plasmin-plasminogen system activation and reduces the 5-oxo-ETE-induced cell migration[3]. Montelukast (10 μM; 18 h) modifies MMP-9 activation[3]. |
|---|---|
| 体外研究 (In Vitro) |
Montelukast（5 μM；1 小时）可抑制 APAP（对乙酰氨基酚）诱导的细胞损伤[1]。孟鲁司特（0.01-10 μM；30 分钟）可减少 5-oxo-ETE 诱导的细胞迁移并调节纤溶酶-纤溶酶原系统的激活[3]。 Montelukast（10 μM；18 小时）调节 MMP-9 的激活[3]。细胞迁移测定 [3] 细胞系：嗜酸性粒细胞 浓度：0.01-10 μM 孵育时间：30 分钟 结果：减少 5-oxo-ETE 诱导的细胞迁移。蛋白质印迹分析[3] 细胞系：嗜酸性粒细胞浓度：10 μM 孵育时间：18 小时 结果：减少 5-oxo-ETE 促进的 MMP-9 分泌。
在原代小鼠肝细胞中，用孟鲁司特 (5 和 10 µM) 预处理可减少对乙酰氨基酚 (APAP, 2.5 mM) 诱导的乳酸脱氢酶 (LDH) 释放。 [1] 孟鲁司特 (5 µM) 能显著逆转APAP诱导的原代小鼠肝细胞线粒体膜电位降低。 [1] 孟鲁司特 抑制了LTD4（一种CysLT1激动剂）诱导的肝细胞损伤。 [1] |
| 体内研究 (In Vivo) |
孟鲁司特（3 mg/kg；口服强饲）可预防小鼠 APAP 诱导的肝毒性[1]。孟鲁司特（1 mg/kg；微渗泵给药）可减少 OVA 治疗小鼠中观察到的气道重塑变化，并阻断 CysLT1 受体介导的半胱氨酰白三烯 (LT) C4、D4 和 E4 的作用[2]。孟鲁司特（1 mg/kg；微渗泵给药）可降低 OVA 治疗小鼠 BAL 液中升高的 IL-4 和 IL-13 水平[2]。动物模型：C57BL/6J 小鼠（8 周龄；22-25 g）诱导急性肝损伤[1] 剂量：3 mg/kg 给药方法：生理盐水或 APAP 给药后 1 小时口服灌胃 结果：血清中丙氨酸转氨酶（ALT）和天冬氨酸转氨酶（AST），并减轻肝脏损伤。
在C57BL/6J小鼠中，于APAP (200 mg/kg) 给药1小时后灌胃给予孟鲁司特 (3 mg/kg)，能显著降低APAP给药12小时后血清中的谷丙转氨酶 (ALT) 和谷草转氨酶 (AST) 水平。 [1] 孟鲁司特 治疗减轻了肝脏损伤，表现为苏木精-伊红 (H&E) 染色肝切片中中央静脉周围坏死面积减少。 [1] 孟鲁司特 治疗上调了APAP给药后3小时肝脏的还原型谷胱甘肽与氧化型谷胱甘肽 (GSH/GSSG) 的比值。 [1] 孟鲁司特 降低了APAP处理小鼠肝脏中过氧化氢 (H2O2) 和硫代巴比妥酸反应物 (TBARS) 的水平，这两种物质是氧化应激的标志物。 [1] 孟鲁司特 抑制了APAP处理小鼠肝脏中炎症细胞因子 (MCP-1、TNF-α、IL-6、IL-1β) 的mRNA表达。 [1] 孟鲁司特 抑制了APAP处理小鼠肝脏中c-Jun N末端激酶 (JNK) 的磷酸化，并轻微抑制了细胞外信号调节激酶 (ERK) 的磷酸化。 [1] |
| 酶活实验 |
孟鲁司特和MK-0591降低了5-氧代-ETE促进的嗜酸性粒细胞迁移，而LTD（4）未能诱导嗜酸性粒细胞核迁移。然而，LTD（4）显著提高了用次优浓度的5-氧代-ETE获得的迁移速率，并部分逆转了用MK-0591获得的抑制作用。孟鲁司特显著降低了用5-氧代-ETE获得的嗜酸性粒细胞将纤溶酶原活化为纤溶酶的最大速率。5-Oxo-ETE增加了表达尿激酶纤溶酶原激活物受体的嗜酸性粒细胞的数量，并刺激了MMP-9的分泌。孟鲁司特，但MK-0591和LTD（4）均未降低尿激酶纤溶酶原激活剂受体的表达和MMP-9的分泌，并增加尿激酶纤溶酶原活化剂的总细胞活性和纤溶酶原激活物抑制剂2mRNA的表达[3]。
|
| 细胞实验 |
细胞系：嗜酸性粒细胞
浓度：0.01-10 μM 孵育时间：30 分钟 结果：减少 5-oxo-ETE 诱导的细胞迁移。 用或不用孟鲁司特治疗纯化的血液嗜酸性粒细胞；MK-0591，一种5-脂氧合酶激活蛋白抑制剂；或白三烯（LT）D（4）。在5-氧代-6,8,11,14-二十碳四烯酸（5-氧代-ETE）（一种强效嗜酸性粒细胞趋化因子或LTD）存在的情况下，通过Matrigel进行迁移测定（4）。还评估了与纤溶酶产生和基质金属蛋白酶（MMP）9释放有关的分子的表达。 结果：孟鲁司特和MK-0591降低了5-氧代-ETE促进的嗜酸性粒细胞迁移，而LTD（4）未能诱导嗜酸性粒血球迁移。然而，LTD（4）显著提高了用次优浓度的5-氧代-ETE获得的迁移率，并部分逆转了用MK-0591获得的抑制作用。孟鲁司特显著降低了5-氧代-ETE获得的嗜酸性粒细胞将纤溶酶原激活为纤溶酶的最大速率。5-Oxo-ETE可增加表达尿激酶型纤溶酶原激活物受体的嗜酸性粒细胞数量，并刺激MMP-9的分泌。孟鲁司特，但MK-0591和LTD（4）均未降低尿激酶纤溶酶原激活物受体的表达和MMP-9的分泌，并增加尿激酶纤溶酶原活化物的总细胞活性和纤溶酶原激活剂抑制剂2 mRNA的表达。 结论：孟鲁司特在体外通过一种可能独立于其对CysLT1受体拮抗作用的机制抑制嗜酸性粒细胞蛋白酶活性[3]。 使用乳酸脱氢酶 (LDH) 细胞毒性检测试剂盒测量细胞死亡。计算释放到培养基中的LDH百分比，相对于用1% Triton X-100处理的细胞（阳性对照）释放的LDH。 [1] 使用JC-1染料检测试剂盒评估线粒体膜电位。细胞与JC-1染料孵育、洗涤后，在荧光显微镜下观察。红色荧光表示高线粒体膜电位（JC-1聚集物），绿色荧光表示低电位（JC-1单体）。 [1] 通过逆转录定量聚合酶链反应 (RT-qPCR) 进行基因表达分析。提取总RNA，逆转录成cDNA，并使用SYBR Green mix进行扩增。靶基因的表达以18S核糖体RNA基因作为内参进行标准化。 [1] 通过蛋白质免疫印迹法分析蛋白表达和磷酸化。肝组织匀浆蛋白经电泳分离，转印至膜上，用针对靶蛋白及其磷酸化形式的特异性一抗孵育，然后用相应的二抗进行检测。 [1] |
| 动物实验 |
C57BL/6J mice (8-week-old; 22-25 g) are induced acute hepatic injury
3 mg/kg Oral gavage 1 h after saline or APAP administration This study used 8-week-old C57BL/6J mice (22–25 g), which were randomly selected for this experimental study. The acute hepatic injury was induced by oral administration of APAP (200 mg/kg) before 16 h fasting as described (Saini et al., 2011; Pu et al., 2016). For therapeutic experiment, a dose of 3 mg/kg (Hamamoto et al., 2017) of Montelukast was prepared in a 0.5% carboxy methyl cellulose. Mice were gavaged in a volume of 100 μl at 1 h after APAP administration. Mice were killed by CO2 at 12 h after APAP administration, and blood and liver tissue were harvested for histology. [1] Female BALB/c mice (aged 6–8 wk) received an intraperitoneal injection of 100 μg of ovalbumin (OVA) complexed with alum on Days 0 and 14. Mice received an intranasal dose of 500 μg OVA on Days 14, 27, 28, 29, 47, 61, 73, 74, and 75. The control group received normal saline with alum intraperitoneally on Days 0 and 14 and saline without alum intranasally on Days 14, 27, 28, 29, 47, 61, 73, 74, and 75. A group of OVA-treated mice was administered the cysteinyl leukotriene1 (CysLT1) receptor antagonist Montelukast sodium (MK-0476) that was dissolved in distilled water containing 10% Na2CO3 (5). Then 200-μl Alzet Model 2004 miniosmotic pumps (6 μl/d delivery rate) containing Montelukast (1 mg/kg) or vehicle control were placed subcutaneously on Day 26 and replaced on Day 54.[2] Eight-week-old male C57BL/6J mice were fasted for 16 hours. [1] Acute liver injury was induced by oral administration (gavage) of acetaminophen (APAP) at a dose of 200 mg/kg. [1] For therapeutic intervention, montelukast was suspended in 0.5% carboxymethyl cellulose and administered by oral gavage at a dose of 3 mg/kg in a volume of 100 µL, 1 hour after APAP administration. [1] Mice were euthanized 12 hours after APAP administration. Blood was collected for serum isolation, and liver tissues were harvested for histological analysis, biochemical assays, and molecular studies. [1] |
| 药代性质 (ADME/PK) |
Absorption, Distribution, and Excretion
Absorption Montelukast is observed to be rapidly absorbed after oral administration. The oral bioavailability of this drug is 64%. Furthermore, it appears that normal morning meals or high-fat snacks in the evening do not affect the absorption of montelukast. Excretion Route Montelukast and its metabolites are reported to be almost entirely excreted via bile and feces. Volume of Distribution The steady-state volume of distribution of montelukast is on average 8 to 11 liters. Clearance The average plasma clearance of montelukast observed in healthy adults is 45 mL/min. Montelukast is rapidly absorbed from the gastrointestinal tract. After oral administration of a single 10 mg film-coated tablet (adult), 5 mg chewable tablet (adult), or 4 mg chewable tablet (child) on an empty stomach, peak plasma concentrations are reached in 3–4 hours, 2–2.5 hours, or 2 hours, respectively. (For children aged 2–5 years) tablets. …When taking the 4 mg oral granules in the morning, consuming a high-fat meal had no effect on the AUC of montelukast; however, the time to peak plasma concentration was prolonged from 2.3 hours to 6.4 hours, and the peak plasma concentration decreased by 35%. Montelukast is rapidly absorbed. The mean oral bioavailability of the 10 mg tablets is 64%. A standard morning meal does not affect bioavailability. For the 5 mg chewable tablets: the mean oral bioavailability on an empty stomach is 73%, while it is 63% when taken with a standard meal in the morning. View MoreIn fasting young adults, after daily oral administration of 10 mg montelukast for 7 consecutive days, the mean peak plasma concentration on day 1 was 541 ng/mL, and the mean peak plasma concentration on day 7 was 602.8 ng/mL. The trough concentrations remained relatively stable from day 3 to day 7, ranging from 18 to 24 ng/mL. In this study, the area under the steady-state plasma concentration-time curve (AUC) was approximately 14-15% higher than that after a single dose, and this was achieved within 2 days. For more complete data on absorption, distribution, and excretion of montelukast (15 items in total), please visit the HSDB record page. Metabolism/Metabolites Montelukast has been identified as actively metabolized, typically by cytochrome P450 3A4, 2C8, and 2C9 isoenzymes. In particular, the CYP2C8 enzyme appears to play a significant role in drug metabolism. However, at therapeutic doses, plasma concentrations of montelukast metabolites are undetectable in both adult and pediatric patients at steady state. Biotransformation occurs primarily in the liver, involving cytochrome P450 3A4 and 2C9. The metabolic pathways of montelukast are not fully understood, but the drug is extensively metabolized in the gastrointestinal tract and/or liver and excreted via bile. Multiple metabolic pathways have been identified, including acyl glucuronidation and oxidation catalyzed by various cytochrome P-450 (CYP) isoenzymes. In vitro studies have shown that the microsomal P-450 isoenzyme CYP3A4 is the major enzyme in the formation of the 21-hydroxy metabolite (M5) and the sulfoxide metabolite (M2), while CYP2C9 is the major isoenzyme in the formation of the 36-hydroxy metabolite (M6). Other identified metabolites include acylglucuronide (M1) and a 25-hydroxy (phenolic, M3) analog. Following oral administration of 54.8 mg of radiolabeled montelukast, drug metabolites account for less than 2% of circulating radioactivity. In radiolabeling studies, montelukast metabolites identified in plasma include 21-hydroxy (benzyl acid diastereomers, M5a and M5b) metabolites and 36-hydroxy (methanol diastereomers, M6a and M6b) metabolites. Following oral administration of a therapeutic dose of montelukast, steady-state plasma metabolite concentrations in both adults and children were below the limit of detection. The known metabolites of montelukast include 21-hydroxymontelukast, 21(S)-hydroxymontelukast, montelukast 1,2-diol, and montelukast sulfoxide. Biological Half-Life Studies have shown that the mean plasma half-life of montelukast in healthy young adults is 2.7 to 5.5 hours. The mean plasma elimination half-life of montelukast in adults aged 19–48 years is 2.7–5.5 hours, with a mean plasma clearance of 45 mL/min. The plasma elimination half-life in children aged 6–14 years is 3.4–4.2 hours. Limited data suggest that the plasma elimination half-life of montelukast is slightly prolonged in older adults and patients with mild to moderate hepatic impairment, but no dose adjustment is required. The plasma elimination half-lives in older adults aged 65–73 years and patients with mild to moderate hepatic impairment have been reported to be 6.6 hours and 7.4 hours, respectively. The standard dose of montelukast for hospitalized COVID-19 patients is 10 mg orally once daily, starting from day 1 of admission [4]. |
| 毒性/毒理 (Toxicokinetics/TK) |
Hepatotoxicity
In clinical trials, mild elevations in serum transaminase (ALT) levels were observed in 1% to 2% of patients taking montelukast long-term, but a similar incidence was reported in the matched placebo group. ALT abnormalities are usually mild, asymptomatic, and self-limiting. Clinically significant liver injury caused by montelukast is rare, but a dozen cases have been reported in the literature. In these cases, the latency period of liver injury varies greatly, ranging from days to years. Patients present with anorexia, nausea, right upper quadrant pain, dark urine, and jaundice. The pattern of enzyme elevation is usually mixed, but hepatocellular or cholestatic patterns have also been reported. Allergic reactions and autoantibody formation are rare. Eosinophilia is common, but this may be due to an underlying allergic disease rather than liver injury. After discontinuation of the drug, the injury usually resolves within 1 to 4 months. Probability score: B (Rare but likely a cause of clinically significant liver injury). Effects during pregnancy and lactation ◉ Overview of medication use during lactation Montallukast is present in extremely low amounts in breast milk. Montelukast is approved for use in infants 6 months and older and has been used in newborns at doses far higher than those found in breast milk. It is expected that the dose ingested by breastfed infants will not cause any adverse effects. International guidelines consider leukotriene receptor antagonists to be safe for use during lactation. ◉ Effects on breastfed infants As of the revision date, no relevant published information was found. ◉ Effects on lactation and breast milk As of the revision date, no relevant published information was found. View More◈ What is Montelukast? Drug Interactions Concomitant use of phenobarbital results in a significant decrease in the area under the curve (AUC) of montelukast (approximately 40%) and induces hepatic metabolism…Thomson/Micromedex. Medical Information for Healthcare Professionals, Vol. 1, Greenwood Village, Colorado, 2007, p. 2030. This study aimed to evaluate whether clinically used dose levels of montelukast interfered with the anticoagulant effect of warfarin. In a two-cycle, double-blind, randomized crossover study, 12 healthy male subjects received a single oral dose of 30 mg warfarin on day 7 of a 12-day montelukast treatment regimen, or montelukast 10 mg orally daily, or placebo. Montelukast had no significant effect on the area under the plasma concentration-time curve (AUC) or peak plasma concentration of either R-warfarin or S-warfarin. However, in the presence of montelukast, a slight but statistically significant reduction was observed in the time to peak concentration of both warfarin enantiomers and the elimination half-life of the less potent R-warfarin. These changes were considered clinically insignificant. Montelukast had no significant effect on the anticoagulant effect of warfarin, as assessed by the international normalized ratio of prothrombin time (INR) (AUC 0-144 and maximum INR). The results of this study suggest that clinically significant drug interactions are unlikely to occur in patients who need to take both drugs concurrently. Protein Binding Montelukast has been found to bind to plasma proteins at a rate exceeding 99%. The most common side effects of montelukast include upper respiratory tract infection, fever, headache, sore throat, and cough. U.S. prescribing information includes a boxed warning about the risk of neuropsychiatric events associated with montelukast[4]. |
| 参考文献 | |
| 其他信息 |
Montelukast sodium is an organic sodium salt containing the montelukast (1-) molecule. Montelukast sodium is a highly bioavailable monosodium salt of montelukast, a selective cysteinyl leukotriene receptor antagonist with anti-inflammatory and bronchodilatory effects. Montelukast selectively and competitively blocks the cysteinyl leukotriene 1 (CysLT1) receptor, thereby preventing the binding of the inflammatory mediator leukotriene D4 (LTD4). Inhibition of LTD4 activity suppresses leukotriene-mediated inflammatory responses, including: eosinophil and neutrophil migration; leukocyte adhesion to vascular endothelial cells; monocyte and neutrophil aggregation; increased airway edema; increased capillary permeability; and bronchoconstriction. CysLT1 receptors are present in a variety of tissues, including the spleen, lungs, placenta, small intestine and nasal mucosa, and in a variety of cell types, including monocytes/macrophages, mast cells, eosinophils, CD34-positive hematopoietic progenitors, neutrophils and endothelial cells. See also: Montelukast (containing the active ingredient). Drug indications Asthma Montelukast is used clinically for the prevention and long-term treatment of asthma. [1] This study showed that montelukast has a protective effect against acute liver injury induced by acetaminophen (APAP) in mice. [1] The hepatoprotective mechanism of montelukast is related to the upregulation of hepatic glutathione levels, the reduction of oxidative stress, the inhibition of JNK signaling pathway and the suppression of inflammatory response. [1] In vivo and in vitro experiments have shown that the expression of CysLT1 receptors in the liver is upregulated after acetaminophen overdose. [1]
|
| 分子式 |
C35H35CLNNAO3S
|
|---|---|
| 分子量 |
608.17
|
| 精确质量 |
607.192
|
| 元素分析 |
C, 69.12; H, 5.80; Cl, 5.83; N, 2.30; Na, 3.78; O, 7.89; S, 5.27
|
| CAS号 |
151767-02-1
|
| 相关CAS号 |
Montelukast; 158966-92-8; Montelukast-d6 sodium; 2673270-26-1; Montelukast dicyclohexylamine; 577953-88-9; Montelukast-d6; 1093746-29-2
|
| PubChem CID |
23663996
|
| 外观&性状 |
White to off-white solid
|
| 沸点 |
750.5ºC at 760mmHg
|
| 熔点 |
115 °C(dec.)
|
| 闪点 |
407.7ºC
|
| LogP |
7.613
|
| tPSA |
98.55
|
| 氢键供体(HBD)数目 |
1
|
| 氢键受体(HBA)数目 |
5
|
| 可旋转键数目(RBC) |
12
|
| 重原子数目 |
42
|
| 分子复杂度/Complexity |
898
|
| 定义原子立体中心数目 |
1
|
| SMILES |
ClC1=CC2=C(C=C1)C=CC(/C=C/C3=CC([C@H](SCC4(CC([O-])=O)CC4)CCC5=CC=CC=C5C(C)(O)C)=CC=C3)=N2.[Na+]
|
| InChi Key |
LBFBRXGCXUHRJY-HKHDRNBDSA-M
|
| InChi Code |
InChI=1S/C35H36ClNO3S.Na/c1-34(2,40)30-9-4-3-7-25(30)13-17-32(41-23-35(18-19-35)22-33(38)39)27-8-5-6-24(20-27)10-15-29-16-12-26-11-14-28(36)21-31(26)37-29;/h3-12,14-16,20-21,32,40H,13,17-19,22-23H2,1-2H3,(H,38,39);/q;+1/p-1/b15-10+;/t32-;/m1./s1
|
| 化学名 |
sodium;2-[1-[[(1R)-1-[3-[(E)-2-(7-chloroquinolin-2-yl)ethenyl]phenyl]-3-[2-(2-hydroxypropan-2-yl)phenyl]propyl]sulfanylmethyl]cyclopropyl]acetate
|
| 别名 |
Montelukast sodium; MK-476; MK476; MK 476; MK-0476; MK 0476; MK0476; Montelukast sodium salt; Montair; Kokast; Montelukast sodium [USAN]; Montelukast (sodium); trade names Singulair; Montelo-10; Monteflo; Lukotas; Lumona
|
| HS Tariff Code |
2934.99.9001
|
| 存储方式 |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month 注意： 请将本产品存放在密封且受保护的环境中，避免吸湿/受潮。 |
| 运输条件 |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
| 溶解度 (体外实验) |
DMSO: 50~100 mg/mL (82.2~164.4 mM)
Water: ~100 mg/mL Ethanol: ~100 mg/mL |
|---|---|
| 溶解度 (体内实验) |
配方 1 中的溶解度: 1.25 mg/mL (2.06 mM) in PBS (这些助溶剂从左到右依次添加，逐一添加), 悬浮液；超声助溶。
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。 |
| 制备储备液 | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.6443 mL | 8.2214 mL | 16.4428 mL | |
| 5 mM | 0.3289 mL | 1.6443 mL | 3.2886 mL | |
| 10 mM | 0.1644 mL | 0.8221 mL | 1.6443 mL |
1、根据实验需要选择合适的溶剂配制储备液 (母液)：对于大多数产品，InvivoChem推荐用DMSO配置母液 (比如：5、10、20mM或者10、20、50 mg/mL浓度），个别水溶性高的产品可直接溶于水。产品在DMSO 、水或其他溶剂中的具体溶解度详见上”溶解度 (体外)”部分;
2、如果您找不到您想要的溶解度信息，或者很难将产品溶解在溶液中，请联系我们;
3、建议使用下列计算器进行相关计算（摩尔浓度计算器、稀释计算器、分子量计算器、重组计算器等）;
4、母液配好之后，将其分装到常规用量，并储存在-20°C或-80°C，尽量减少反复冻融循环。
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)。如该浓度超过该批次药物DMSO溶解度，请首先与我们联系。
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 ddH2O，混匀澄清。
(1) 请确保溶液澄清之后，再加入下一种溶剂 (助溶剂) 。可利用涡旋、超声或水浴加热等方法助溶；
(2) 一定要按顺序加入溶剂 (助溶剂) 。
The Singulair® add-on Study Effectiveness of Adding Montelukast to Inhaled Corticosteroids in Adult Subjects With Uncontrolled Asthma (0476-384)
CTID: NCT00755794
Phase: Phase 3 Status: Completed
Date: 2024-06-07
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