| 规格 | 价格 | 库存 | 数量 |
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| 500mg |
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| 1g |
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| 2g |
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| 5g |
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| Other Sizes |
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| 靶点 |
CysLT1 (cysteinyl leukotriene receptor 1)
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| 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。
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| 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。
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| 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]。
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| 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。
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| 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 |
| 药代性质 (ADME/PK) |
Absorption, Distribution and Excretion
Absorption It has been observed that montelukast is quickly absorbed following administration by the oral route. The oral bioavailability documented for the drug is 64%. Furthermore, it seems that having a regular meal in the morning or even a high fat snack in the evening does not affect the absorption of montelukast. Route of Elimination It has been reported that montelukast and its metabolites are almost exclusively excreted in the bile and into the feces. Volume of Distribution The steady-state volume of distribution recorded for montelukast is an average between 8 to 11 litres. Clearance The plasma clearance documented for montelukast is an average of 45 mL/min when observed in healthy adults. Montelukast is rapidly absorbed from the GI tract, and peak plasma concentrations are attained within 3-4, 2-2.5, or 2 hours following oral administration in the fasted state of a single 10-mg film-coated (in adults), 5-mg chewable (in adults), or 4-mg chewable (in children 2-5 years of age) tablet, respectively. ... Ingestion of a high-fat meal in the morning with the 4-mg oral granules formulation had no effect on the AUC of montelukast; however, the time to peak plasma concentrations was prolonged from 2.3 hours to 6.4 hours and peak plasma concentrations were reduced by 35%. Absorption /of montelukast is/ rapid. For the 10-mg tablets: mean oral bioavailability is 64%. Bioavailability is not affected by a standard meal in the morning. For the 5-mg chewable tablet: mean oral bioavailability is 73% in the fasted state versus 63% when administered with a standard meal in the morning. View More
Following oral administration of montelukast 10 mg daily for 7 days in fasting young adults, peak plasma concentrations averaged 541 ng/mL on day 1 and 602.8 ng/mL on day 7. Trough concentrations on days 3-7 were essentially constant and ranged from 18-24 ng/mL. In this study, values for area under the plasma concentration-time curve (AUC) at steady-state were about 14-15% higher than those achieved with a single dose, and were reached within 2 days.
Metabolism / Metabolites It has been determined that montelukast is highly metabolized and typically so by the cytochrome P450 3A4, 2C8, and 2C9 isoenzymes. In particular, it seems that the CYP2C8 enzymes play a significant role in the metabolism of the drug. Nevertheless, at therapeutic doses, the plasma concentrations of montelukast metabolites are undetectable at steady state in adults and pediatric patients. Biotransformation /is/ hepatic and extensive involving cytochrome P450 3A4 and 2C9 The metabolic fate of montelukast has not been fully determined, but the drug is extensively metabolized in the GI tract and/or liver and excreted in bile. Several metabolic pathways have been identified including acyl glucuronidation, and oxidation catalyzed by several cytochrome P-450 (CYP) isoenzymes. In vitro studies indicate that the microsomal P-450 isoenzyme CYP3A4 is the major enzyme involved in formation of the 21-hydroxy metabolite (M5) and a sulfoxide metabolite (M2), and CYP2C9 is the major isoenzyme involved in the formation of the 36-hydroxy metabolite (M6). Other identified metabolites include an acyl glucuronide (M1) and a 25-hydroxy (a phenol, M3) analog. Following oral administration of 54.8 mg of radiolabeled montelukast, metabolites of the drug represented less than 2% of circulating radioactivity. Montelukast metabolites that have been identified in plasma in radiolabeled studies include the 21-hydroxy (diastereomers of a benzylic acid, M5a and M5b) and the 36-hydroxy (diastereomers of a methyl alcohol, M6a and M6b) metabolites. Following oral administration of therapeutic doses of montelukast, plasma concentrations of metabolites at steady-state in adults and children were below the level of detection. Montelukast has known human metabolites that include 21-Hydroxymontelukast, 21(S)-Hydroxy Montelukast, Montelukast 1, 2-Diol, and montelukast sulfoxide. Biological Half-Life Studies have demonstrated that the mean plasma half-life of montelukast varies from 2.7 to 5.5 hours when observed in healthy young adults. The mean plasma elimination half-life of montelukast in adults 19-48 years of age is 2.7-5.5 hours, and plasma clearance averages 45 mL/minute. A plasma elimination half-life of 3.4-4.2 hours has been reported in children 6-14 years of age. Limited data indicate that the plasma elimination half-life of montelukast is prolonged slightly in geriatric adults and in patients with mild to moderate hepatic impairment, although dosage adjustment is not required. A plasma elimination half-life of 6.6 or 7.4 hours has been reported in geriatric adults 65-73 years of age or patients with mild to moderate hepatic impairment, respectively. |
| 毒性/毒理 (Toxicokinetics/TK) |
Hepatotoxicity
In clinical trials, mild elevations in serum aminotransferase levels were found in 1% to 2% of patients taking montelukast chronically, but similar rates are reported in matched placebo recipients. The ALT abnormalities were usually mild, asymptomatic and self limited. Clinically apparent liver injury from montelukast is rare; but more than a dozen cases reported in the literature. In these cases, the latency to onset of injury was highly variable, ranging from a few days to several years. Patients presented with anorexia, nausea, right upper quadrant pain, dark urine, and jaundice. The pattern of enzyme elevation was usually mixed, but both hepatocellular or cholestatic patterns have been reported. Allergic features and autoantibody formation were rare. Eosinophilia was often reported, but this may have been due to the underlying allergic condition rather than the liver injury. The injury usually resolved within 1 to 4 months of stopping the drug. Likelihood score: B (rare but likely cause of clinically apparent liver injury). Effects During Pregnancy and Lactation ◉ Summary of Use during Lactation Very low levels of montelukast appear in breastmilk. Montelukast is approved for use in children as young as 6 months of age and has been used in neonates in dosages far greater than the amounts in breastmilk. Amounts ingested by the infant would not be expected to cause any adverse effects in breastfed infants. International guidelines consider that leukotriene receptor antagonists can be used during breastfeeding. ◉ 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. View More
◈ What is montelukast?
Interactions Concurrent use /of phenobarbital/ results in significant decreases (approximately 40%) in the area under the curve [AUC] for montelukast, of induction of hepatic metabolism... Thomson/Micromedex. Drug Information for the Health Care Professional. Volume 1, Greenwood Village, CO. 2007., p. 2030 ... This study was designed to evaluate whether montelukast at clinically used dosage levels would interfere with the anticoagulant effect of warfarin. In a two-period, double-blind, randomized crossover study, 12 healthy male subjects received a single oral dose of 30 mg warfarin on the 7th day of a 12-day treatment with montelukast, 10 mg daily by mouth, or a placebo. Montelukast had no significant effect on the area under the plasma concentration-time curves and peak plasma concentrations of either R- or S-warfarin. However, slight but statistically significant decreases in time to peak concentration of both warfarin enantiomers and in elimination half-life of the less potent R-warfarin were observed in the presence of montelukast. These changes were not considered as clinically relevant. Montelukast had no significant effect on the anticoagulant effect of warfarin, as assessed by the international normalized ratio (INR) for prothrombin time (AUC0-144 and INR maximum). The results of this study suggest that a clinically important interaction between these drugs is unlikely to occur in patients requiring concomitant administration of both drugs. Protein Binding It has been determined that the protein binding of montelukast to plasma proteins exceeds 99%. |
| 参考文献 | |
| 其他信息 |
Montelukast is a member of quinolines, a monocarboxylic acid and an aliphatic sulfide. It has a role as a leukotriene antagonist, an anti-asthmatic drug and an anti-arrhythmia drug. It is a conjugate acid of a montelukast(1-).
Montelukast was first approved for clinical use by the US FDA in 1998 as Merck's brand name Singulair. The medication is a member of the leukotriene receptor antagonist (LTRA) category of drugs. Although capable of demonstrating effectiveness, the use of such LTRAs like montelukast is typically in addition to or complementary with the use of inhaled corticosteroids or other agents in asthma step therapy. Regardless, in 2008-2009, there were FDA-led investigations into the possibility of montelukast to elicit neuropsychiatric effects like agitation, hallucinations, suicidal behaviour, and others in individuals who used the medication. And although these kinds of effects are currently included in the official prescribing information for montelukast, the drug still sees extensive use worldwide via millions of prescriptions annually and has since become available as a generic and as a brand name product. Montelukast is a Leukotriene Receptor Antagonist. The mechanism of action of montelukast is as a Leukotriene Receptor Antagonist. Montelukast is an orally available leukotriene receptor antagonist which is widely used for the prophylaxis and chronic treatment of asthma and has been linked to rare cases of clinically apparent liver injury. Montelukast is a selective cysteinyl leukotriene receptor antagonist with anti-inflammatory and bronchodilating activities. Upon administration, montelukast selectively and competitively blocks the cysteinyl leukotriene 1 (CysLT1) receptor, preventing binding of the inflammatory mediator leukotriene D4 (LTD4). Inhibition of LTD4 activity results in inhibition of leukotriene-mediated inflammatory events including migration of eosinophils and neutrophils, adhesion of leukocytes to vascular endothelium, monocyte and neutrophil aggregation, increased airway edema, increased capillary permeability, and bronchoconstriction. The CysLT1 receptor is found in a number of tissues including spleen, lung, placenta, small intestine, and nasal mucosa, and in a variety of cell types including monocyte/macrophages, mast cells, eosinophils, CD34-positive hemopoietic progenitor cells, neutrophils and endothelial cells. View More
Drug Indication
Therapeutic Uses Anti-Asthmatic agents; Leukotriene Antagonists Montelukast is indicated for prophylaxis and chronic treatment of asthma in adults and pediatric patients 12 months of age and older. /Included in US product label/ Drug Warnings Headache is the most frequently reported adverse effect with montelukast, occurring in 18-19% of children 6 years of age or older, adolescents, and adults. Headache has been reported in at least 2% of children 2-8 years of age with asthma receiving montelukast and in at least 1% (and more frequently than with placebo) of adults and adolescents 15 years of age or older with asthma. Sinus headache has been reported in at least 1% of adult and adolescent patients 15 years of age or older with perennial allergic rhinitis receiving montelukast and more frequently than in those receiving placebo. Dizziness or asthenia/fatigue has occurred in about 1.8-1.9% of patients 15 years of age or older receiving the drug in clinical studies. Dream abnormalities, hallucinations, agitation including aggressive behavior, paresthesia/hypoesthesia, drowsiness, insomnia, irritability, or restlessness also has been reported; seizures have been reported very rarely. Abdominal pain has occurred in 2.9% of patients 15 years of age or older receiving montelukast. Dyspepsia, infectious gastroenteritis, and dental pain have been reported in 2.1, 1.5, and 1.7% of patients in this age group, respectively. Diarrhea or nausea has been reported in at least 2% of children 6-14 years of age receiving montelukast. Abdominal pain, diarrhea, and gastroenteritis has been reported in at least 2% of children 2-5 years of age with asthma and more frequently than in those receiving placebo. Gastroenteritis has been reported in at least 2% of children 6-8 years of age with asthma and more frequently than in those receiving placebo. Nausea, vomiting, dyspepsia, pancreatitis (rarely), and diarrhea also have been reported with montelukast therapy during postmarketing experience. Pharmacodynamics Montelukast is a leukotriene receptor antagonist that demonstrates a marked affinity and selectivity to the cysteinyl leukotriene receptor type-1 in preference to many other crucial airway receptors like the prostanoid, cholinergic, or beta-adrenergic receptors. As a consequence, the agent can elicit substantial blockage of LTD4 leukotriene-mediated bronchoconstriction with doses as low as 5 mg. Moreover, a placebo-controlled, crossover study (n=12) demonstrated that montelukast is capable of inhibiting early and late phase bronchoconstriction caused by antigen challenge by 75% and 57% respectively. In particular, it has been documented that montelukast can cause bronchodilation as soon as within 2 hours of oral administration. This action can also be additive to the bronchodilation caused by the concomitant use of a beta agonist. Nevertheless, clinical investigations performed with adults 15 years of age and older revealed that no additional clinical benefit is obtained when doses of montelukast greater than 10 mg a day are used. Additionally, in clinical trials with adults and pediatric asthmatic patients aged 6 to 14 years, it was also determined that montelukast can reduce mean peripheral blood eosinophils by about 13% to 15% from baseline in comparison to placebo during double-blind treatment periods. At the same time, in patients aged 15 years and older who were experiencing seasonal allergic rhinitis, the use of montelukast caused a median reduction of 13% in peripheral blood eosinophil counts when compared to placebo as well. Mechanism of Action Cysteinyl leukotrienes (CysLT) like LTC4, LTD4, and LTE4, among others, are eicosanoids released by a variety of cells like mast cells and eosinophils. When such CysLT bind to corresponding CysLT receptors like CysLT type-1 receptors located on respiratory airway smooth muscle cells, airway macrophages, and on various pro-inflammatory cells like eosinophils and some specific myeloid stem cells activities that facilitate the pathophysiology of asthma and allergic rhinitis are stimulated. In particular, CysLT-mediated airway bronchoconstriction, occluding mucous secretion, vascular permeability, and eosinophil recruitment are all types of effects that facilitate asthma. Alternatively, in allergic rhinitis, CysLTs are released by the nasal mucosa when exposed to allergens during both early and late phase reactions and participate in eliciting symptoms of allergic rhinitis like a congested nose and airway. Subsequently, montelukast is a leukotriene receptor antagonist that binds with high affinity and selectivity to the CysLT type 1 receptor, which consequently assists in inhibiting any physiological actions of CysLTs like LTC4, LTD4, and LTE4 at the receptor that may facilitate asthma or allergic rhinitis. Montelukast inhibits bronchoconstriction due to antigen challenge. Montelukast is a selective leukotriene receptor antagonist of the cysteinyl leukotriene CysLT1 receptor. The cysteinyl leukotrienes (LTC4 , LTD4, LTE4) are products of arachidonic acid metabolism that are released from various cells, including mast cells and eosinophils. They bind to cysteinyl leukotriene receptors (CysLT) found in the human airway. Binding of cysteinyl leukotrienes to leukotriene receptors has been correlated with the pathophysiology of asthma, including airway edema, smooth muscle contraction, and altered cellular activity associated with the inflammatory process, factors that contribute to the signs and symptoms of asthma. Montelukast binding to the CysLT1, receptor is high-affinity and selective, preferring the CysLT1 receptor to other pharmacologically important airway receptors, such as the prostanoid, cholinergic, or beta-adrenergic receptor. Montelukcast inhibits physiologic actions of LTD4 at the CysLT1 receptors, without any agonist activity. Thomson/Micromedex. Drug Information for the Health Care Professional. Volume 1, Greenwood Village, CO. 2007., p. 2029 Because of the role of leukotrienes in the pathogenesis of asthma, modification of leukotriene activity may be used to reduce airway symptoms, decrease bronchial smooth muscle tone, and improve asthma control. Inhibition of leukotriene-mediated effects may be achieved by drugs that interrupt 5-lipoxygenase activity and prevent formation of leukotrienes (e.g., zileuton) or by antagonism of leukotriene activity at specific receptor sites in the airway (e.g., montelukast, zafirlukast). The antagonist activity of montelukast is selective, competitive, and reversible. Montelukast competitively inhibits the action of LTD4 at a subgroup of CysLT receptors (CysLT1) in airway smooth muscle. In vitro, montelukast possesses affinity for the CysLT1 receptor that is similar to that of LTD4. In in vitro studies, montelukast antagonized contraction of isolated animal smooth muscle produced by LTD4, but did not antagonize contraction produced by LTC4. In animal studies, montelukast antagonized contraction of airway smooth muscle produced by LTD4 or antigen. |
| 分子式 |
C47H59CLN2O3S
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|---|---|
| 分子量 |
767.50096
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| 精确质量 |
766.393
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| CAS号 |
577953-88-9
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| 相关CAS号 |
Montelukast sodium; 151767-02-1; Montelukast; 158966-92-8
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| PubChem CID |
16202490
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| 外观&性状 |
White to off-white solid powder
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| 熔点 |
65-67°C (lit.)
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| LogP |
12.58
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| tPSA |
107.75
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| 氢键供体(HBD)数目 |
3
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| 氢键受体(HBA)数目 |
6
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| 可旋转键数目(RBC) |
14
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| 重原子数目 |
54
|
| 分子复杂度/Complexity |
1010
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| 定义原子立体中心数目 |
1
|
| SMILES |
CC(C)(C1=CC=CC=C1CC[C@H](C2=CC=CC(=C2)/C=C/C3=NC4=C(C=CC(=C4)Cl)C=C3)SCC5(CC5)CC(=O)O)O.C1CCC(CC1)NC2CCCCC2
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| InChi Key |
ZLOLVGQQYDQBMP-HKHDRNBDSA-N
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| InChi Code |
InChI=1S/C35H36ClNO3S.C12H23N/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;1-3-7-11(8-4-1)13-12-9-5-2-6-10-12/h3-12,14-16,20-21,32,40H,13,17-19,22-23H2,1-2H3,(H,38,39);11-13H,1-10H2/b15-10+;/t32-;/m1./s1
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| 化学名 |
2-[1-[[(1R)-1-[3-[(E)-2-(7-chloroquinolin-2-yl)ethenyl]phenyl]-3-[2-(2-hydroxypropan-2-yl)phenyl]propyl]sulfanylmethyl]cyclopropyl]acetic acid;N-cyclohexylcyclohexanamine
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| 别名 |
Montelukast dicyclohexylamine; Montelukast Dicyclohexylamine Salt; 577953-88-9; Montelukast (dicyclohexylamine); Montelukast dicyclohexylamine; 2-[1-[[(1R)-1-[3-[(E)-2-(7-chloroquinolin-2-yl)ethenyl]phenyl]-3-[2-(2-hydroxypropan-2-yl)phenyl]propyl]sulfanylmethyl]cyclopropyl]acetic acid;N-cyclohexylcyclohexanamine; Montelukast DCHA; Montelukastdicyclohexylamine; SCHEMBL919528; MK0476 dicyclohexylamine
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| HS Tariff Code |
2934.99.9001
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| 存储方式 |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| 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)
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| 溶解度 (体外实验) |
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
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|---|---|
| 溶解度 (体内实验) |
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。
注射用配方
注射用配方1: DMSO : Tween 80： Saline = 10 : 5 : 85 (如： 100 μL DMSO → 50 μL Tween 80 → 850 μL Saline)(IP/IV/IM/SC等) *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。 View More
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)] 口服配方
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。 View More
口服配方 3: 溶解于 PEG400 (聚乙二醇400) 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 | 1.3029 mL | 6.5147 mL | 13.0293 mL | |
| 5 mM | 0.2606 mL | 1.3029 mL | 2.6059 mL | |
| 10 mM | 0.1303 mL | 0.6515 mL | 1.3029 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) 。
| NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
| NCT00934713 | COMPLETED | Drug: montelukast | Lung Disease, Obstructive Signs and Symptoms, Respiratory |
University of Helsinki | 2004-09 | Phase 4 |
| NCT00453765 | COMPLETED | Drug: montelukast Drug: placebo |
Bronchial Hyperreactivity Cough |
Isala | 2007-12 | Phase 4 |
| NCT02029313 | COMPLETED | Drug: Montelukast Drug: Montelukast sodium |
Asthma and Allergic Rhinitis | PharmaKing | 2013-11 | Phase 1 |
| NCT02793375 | ACTIVE, NOT RECRUITING | Drug: Montelukast Drug: Placebo |
Pain | Children's Hospital Medical Center, Cincinnati | 2018-08-02 | Phase 3 |
| NCT00565955 | COMPLETED | Drug: montelukast Drug: Placebo |
Bronchial Asthma | All India Institute of Medical Sciences, New Delhi | 2007-03 | Phase 3 |
|
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Pobilukast
REV 5901 hydrochloride
Pirodomast
CysLT1 receptor antagonist-1
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