MONTELUKAST SODIUM (MK0476) 中文名称: 孟鲁司特钠

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 孟鲁司特钠; 孟鲁斯特钠; 孟鲁司特钠水合物; Montelukast Sodium Hydrate 孟鲁司特钠水合物; 孟鲁司特-D6钠;孟鲁司特峰鉴别 EP标准品;孟鲁司特钠 EP标准品;孟鲁司特钠 USP标准品;孟鲁司特钠标准品;孟鲁司特钠 ;孟鲁司特钠(治哮喘);孟鲁司特钠盐; 孟鲁司特钠原药; 孟鲁司特钠杂质对照品; 孟鲁斯特纳;孟鲁斯特钠标准品;[R-(E)]-1-[[[1-[3-[2-(7-氯-2-喹啉)乙烯基]苯基-3-[2-(1-羟基-1-甲基乙基)苯基]丙基]硫]甲基]环丙烷乙酸钠

目录号: V4387 纯度: ≥98%

COA 产品数据产品说明书 SDS

孟鲁司特钠（也称为 MK-476；商品名 Singulair、Monteflo、Lukotas、Lumona）是一种新型、强效、选择性 CysLT1（白三烯受体）受体拮抗剂，用于哮喘的维持治疗和缓解季节性过敏症状。

MONTELUKAST SODIUM (MK0476) CAS号: 151767-02-1
产品类别: Leukotriene Receptor

产品仅用于科学研究，不针对患者销售

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10 mM * 1 mL in DMSO
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InvivoChem产品被CNS等顶刊论文引用

Nature 2021, 597(7874):119-125.

Cell 2020,183:1202-1218.e25.

Science Adv 2022: 8, eabm9427.

Nature 597, 119–125 (2021)

Cell Stem Cell 2020,26(6):845-861.e12.

Science Trans Med 2023,15(701):eadd7872.

STTT 2023,8(1):91.

Cell Reports 2023,42(4):112313

Science Trans Med 2023, 15: eadd7872.

Cancer Cell 2021,39(4):529-547.e7.

Cancer Discov 2022,12(4):1106-1127.

Immunity 2023,56(3):620-634.e11.

J Am Chem Soc 2022,144:21831-21836.

Cell 2020,183:1202-1218.e25.

Science Adv 2022:8,eabm9427.

Nature 2021,597(7874):119-125.

Cell 2020,183:1202-1218.e25.

PNAS Nexus 2022,1(3):pgac063.

ACS Nano 2023,17(10):9110-9125.

Biomaterial 2023 Sep16:302:122333.

纯度/质量控制文件

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纯度: ≥98%

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产品描述
生物活性&实验参考方法
化学信息
溶解度数据
计算器
临床试验信息
生物数据图片
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产品描述

孟鲁司特钠（也称为 MK-476；商品名 Singulair、Monteflo、Lukotas、Lumona）是一种新型、有效、选择性 CysLT1（白三烯受体）受体拮抗剂，用于哮喘的维持治疗和缓解季节性过敏症状。孟鲁司特通过与肺部和支气管中的半胱氨酰白三烯受体 CysLT1 结合，阻断白三烯 D4（以及二级配体 LTC4 和 LTE4）对其的作用。这减少了白三烯引起的支气管收缩，并减少炎症。

生物活性&实验参考方法

靶点	CysLT₁/cysteinyl leukotriene receptor 1
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。
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。
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]。
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]
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. The pharmacokinetics of montelukast are nearly linear at doses of up to 50 mg. For more Absorption, Distribution and Excretion (Complete) data for MONTELUKAST (15 total), please visit the HSDB record page. 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? Montelukast is medication used to treat asthma and allergies. Montelukast works by blocking a group of chemicals in the body called leukotrienes. Leukotrienes cause inflammation (swelling) of the airways, which can make it hard to breathe. Montelukast is used to help control allergy symptoms and to lower the chance of having an asthma attack. It is not used to stop an asthma attack. Montelukast is sold under the brand name Singulair®.Sometimes when people find out they are pregnant, they think about changing how they take their medication, or stopping their medication altogether. However, it is important to talk with your healthcare providers before making any changes to how you take this medication. Your healthcare providers can talk with you about the benefits of treating your condition and the risks of untreated illness during pregnancy.It is important to think about the benefits of controlling asthma symptoms during pregnancy. Untreated asthma increases the chance for complications for the person who is pregnant as well as the baby. For more information, please see the MotherToBaby fact sheet on asthma at https://mothertobaby.org/fact-sheets/asthma-and-pregnancy/. ◈ I take montelukast. Can it make it harder for me to get pregnant? Studies have not been done in humans to see if montelukast can make it harder to get pregnant. Animal studies showed no effect on fertility. ◈ Does taking montelukast increase the chance for miscarriage? Miscarriage can occur in any pregnancy. Based on the studies reviewed, it is not known if montelukast increases the chance for miscarriage. One study did not show an increase in the rate of miscarriage with use of montelukast during pregnancy. ◈ Does taking montelukast increase the chance of birth defects? Every pregnancy starts out with a 3-5% chance of having a birth defect. This is called the background risk.The manufacturer of montelukast reported a possible link between the use of montelukast during pregnancy and limb defects (problems with fingers, toes, arms or legs). However, only 6 cases of limb defects were reported. The types of limb defects in the report were different from one another, which suggest they do not have a common cause (such as an exposure to a particular medication). Also, these children were exposed to other medications during pregnancy. The label for montelukast notes that the reports did not prove that use of montelukast in pregnancy caused the reported limb defects.Medical record reviews of thousands of pregnancies reportedly exposed to montelukast did not find an increased chance of limb defects or other birth defects. Other studies looking at a combined total of over 200 pregnancies exposed to montelukast have not suggested an increased chance for birth defects. In summary, based on the studies reviewed, the use of montelukast during pregnancy is not expected to increase the chance of birth defects above the background risk. ◈ Does taking montelukast in pregnancy increase the chance of other pregnancy-related problems? A few studies have reported a chance for some pregnancy complications when montelukast was used during pregnancy, such as: lower birth weight, preterm delivery (delivery before 37 weeks of pregnancy), and preeclampsia (a disorder that can cause high blood pressure and protein in the urine in the person who is pregnant). However, these could also be the due to more severe or poorly controlled asthma and not the montelukast itself. The people in these studies who needed montelukast often had severe asthma and sometimes needed more than one medication. It is not clear if the reported complications are due to montelukast, more severe or poorly controlled asthma, or other factors. One study did not notice a difference in birth weight of babies exposed to montelukast when compared to babies exposed to other asthma treatments. ◈ Does taking montelukast in pregnancy affect future behavior or learning for the child? Studies have not been done to see if montelukast can cause behavior or learning issues for the child. ◈ Breastfeeding while taking montelukast: Montelukast gets into breastmilk in small amounts. One study found that nursing infants would likely receive less of the medication in breastmilk than the dose used to treat an infant directly. Usually, no special precautions are required when using montelukast while breastfeeding. Be sure to talk to your healthcare provider about all of your breastfeeding questions. ◈ If a male takes montelukast, could it affect fertility (ability to get partner pregnant) or increase the chance of birth defects? Studies have not been done to see if montelukast could affect human fertility or increase the chance of birth defects. Animal studies showed no effects on fertility. In general, exposures that fathers or sperm donors have are unlikely to increase the risks to a pregnancy. For more information, please see the MotherToBaby fact sheet on Paternal Exposures at https://mothertobaby.org/fact-sheets/paternal-exposures-pregnancy/. 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	[1]. Montelukast Prevents Mice Against Acetaminophen-Induced Liver Injury. Front Pharmacol. 2019 Sep 18; 10:1070. [2]. A role for cysteinyl leukotrienes in airway remodeling in a mouse asthma model. Am J Respir Crit Care Med. 2002 Jan 1; 165(1): 108-16. [3]. Montelukast regulates eosinophil protease activity through a leukotriene-independent mechanism. J Allergy Clin Immunol. 2006;118(1):113-119. [4]. Montelukast in hospitalized patients diagnosed with COVID-19. J Asthma. 2022 Apr;59(4):780-786.
其他信息	Montelukast sodium is an organic sodium salt. It contains a montelukast(1-). Montelukast Sodium is the orally bioavailable monosodium salt of montelukast, a selective cysteinyl leukotriene receptor antagonist with anti-inflammatory and bronchodilating activities. 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. See also: Montelukast (has active moiety). Drug Indication Asthma

*注: 文献方法仅供参考, InvivoChem并未独立验证这些方法的准确性

化学信息 & 存储运输条件

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)

溶解度数据

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。

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。

计算器

质量

浓度

体积

分子量*

计算重置

摩尔浓度计算器可计算特定溶液所需的质量、体积/浓度，具体如下：

计算制备已知体积和浓度的溶液所需的化合物的质量
计算将已知质量的化合物溶解到所需浓度所需的溶液体积
计算特定体积中已知质量的化合物产生的溶液的浓度

参见示例

使用摩尔浓度计算器计算摩尔浓度的示例如下所示：
假如化合物的分子量为350.26 g/mol，在5mL DMSO中制备10mM储备液所需的化合物的质量是多少？

在分子量（MW）框中输入350.26
在“浓度”框中输入10，然后选择正确的单位（mM）
在“体积”框中输入5，然后选择正确的单位（mL）
单击“计算”按钮
答案17.513 mg出现在“质量”框中。以类似的方式，您可以计算体积和浓度。

浓度 (起始)

体积 (起始)

浓度 (终)

体积 (终)

计算重置

稀释计算器可计算如何稀释已知浓度的储备液。例如，可以输入C1、C2和V2来计算V1，具体如下：

制备25毫升25μM溶液需要多少体积的10 mM储备溶液？
使用方程式C1V1=C2V2，其中C1=10mM，C2=25μM，V2=25 ml，V1未知：

在C1框中输入10，然后选择正确的单位（mM）
在C2框中输入25，然后选择正确的单位（μM）
在V2框中输入25，然后选择正确的单位（mL）
单击“计算”按钮
答案62.5μL（0.1 ml）出现在V1框中

分子式

分子量

g/mol

计算重置

分子量计算器可计算化合物的分子量 (摩尔质量)和元素组成，具体如下：

注：化学分子式大小写敏感：C12H18N3O4 c12h18n3o4
计算化合物摩尔质量（分子量）的说明：

要计算化合物的分子量 (摩尔质量)，请输入化学/分子式，然后单击“计算”按钮。

分子质量、分子量、摩尔质量和摩尔量的定义：

分子质量（或分子量）是一种物质的一个分子的质量，用统一的原子质量单位（u）表示。（1u等于碳-12中一个原子质量的1/12）
摩尔质量（摩尔重量）是一摩尔物质的质量，以g/mol表示。

配液体积

质量

配液浓度

计算重置

配液计算器可计算将特定质量的产品配成特定浓度所需的溶剂体积 (配液体积)

输入试剂的质量、所需的配液浓度以及正确的单位
单击“计算”按钮
答案显示在体积框中

动物体内实验配方计算器（澄清溶液）

第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量）

给药剂量 mg/kg

动物平均体重 g

每只动物给药体积 μL

动物数量

第二步：请输入动物体内配方组成（配方适用于不溶/难溶于水的化合物），不同的产品和批次配方组成不同，如对配方有疑问，可先联系我们提供正确的体内实验配方。此外，请注意这只是一个配方计算器，而不是特定产品的确切配方。

% DMSO

% Tween 80

% ddH₂O

计算重置

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。

注意： (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) 。

临床试验信息

NCT Number	Recruitment	interventions	Conditions	Sponsor/Collaborators	Start Date	Phases
NCT04613180	Active Recruiting	Drug: Montelukast Sodium Drug: Placebo	Acute Bronchiolitis	Samarkand State Medical Institute	January 3, 2018	Phase 4
NCT05894577	Active Recruiting	Other: Placebo Drug: Montelukast	Covid19	Susanna Naggie, MD	January 27, 2023	Phase 3
NCT04885530	Active Recruiting	Drug: Fluticasone Other: Placebo Drug: Montelukast Drug: Metformin	Covid19	Susanna Naggie, MD	June 8, 2021	Phase 3
NCT05607446	Recruiting	Drug: TQC3564 tablets Drug: Placebo tablets	Allergic Rhinitis Drug: T	Chia Tai Tianqing Pharmaceutical Group Co., Ltd.	September 14, 2022	Phase 1
NCT04572256	Recruiting	Drug: Montelukast Drug: Placebo	ACL Injury Meniscus Tear	Austin V Stone	February 1, 2021	Early Phase 1

生物数据图片

Montelukast treatment maintained hepatic GSH level and reduced reactive oxygen species production in APAP treated mice. Front Pharmacol . 2019 Sep 18:10:1070.
Montelukast inhibit APAP-induced cell damage. Front Pharmacol . 2019 Sep 18:10:1070.