N-methyl Leukotriene C4 - CAS:131391-65-6

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N-methyl Leukotriene C4 (Synonyms:N-Methyl-LTC4)

目录号 : KCM11008 CAS No. : 131391-65-6 纯度 : ≥97%

Data Sheet 产品使用指南

Produced by neutrophils, macrophages, mast cells, and by transcellular metabolism in platelets, leukotriene C (LTC) is the parent cysteinyl leukotriene formed by the LTC synthase-catalyzed conjugation of glutathione to LTA It is one of the constituents of slow-reacting substance of anaphylaxis (SRS-A) and exhibits potent smooth muscle contracting activity. LTC, however, is rapidly metabolized to LTD and LTE, which makes the characterization of LTC pharmacology difficult. N-methyl Leukotriene C (N-methyl LTC) is a synthetic analog of LTC that is not readily metabolized to LTD and LTEIt acts as a potent and selective CysLT receptor agonist exhibiting EC values of 122 and > 2,000 nM at the human CysLT and CysLT receptors, respectively. It has essentially the same potency as LTC at both the human and murine receptors CysLT receptors. N-methyl LTC is potent and active in vivo, causing vascular leak in mice overexpressing the human CysLT receptor but not in CysLT receptor knockout mice.

规格	价格	是否有货	数量
25μg		In-stock
50μg		In-stock
100μg		In-stock

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生物活性

N-methyl Leukotriene C4 is a non-metabolizable LTC4 analog and a selective cysteinyl leukotriene receptor 2 (CysLT2) agonist, with an EC₅₀ of 46.1 nM for mouse CysLT2 and an EC₅₀ value of 122.3 nM for human CysLT2. N-Methyl Leukotriene C4 shows low potency against CysLT1. N-Methyl Leukotriene C4 activates human and mouse CysLT2 receptors, triggering calcium signaling, β-arrestin-2 binding to phosphorylated receptors, vascular leakage, hypotension, tachycardia, contraction of guinea pig ileum and trachea, mild bronchoconstriction, as well as hypertension associated with peripheral vasoconstriction. N-Methyl Leukotriene C4 can be used in research on asthma, rhinitis, sinusitis, cerebral inflammation and edema, pulmonary arterial hypertension, and cardiovascular diseases.

体外研究

N-Methyll Leukotriene C4 (3 μM; 1 h, 30 s) can serve as a fully potent agonist of the human CysLT2 receptor in HEK 293 cells, with an EC50 of 122.3 nM, reaching 98% of the maximum efficacy of LTC4 [1].

N-MethylLeukotriene C4 (serial diluents, 1.5 μM; 1 h, 30 s) is a fully potent agonist of the mouse CysLT2 receptor in HEK 293 cells, with an EC50 of 46.1 nM, reaching 89% of the maximum efficacy of LTC4 [1].

N-Methyll Leukotriene C4 (10-40 μM; 1 h, 30 s) is a very weak partial agonist of the human CysLT1 receptor, acting on HEK 293 cells with an EC50 ≥ 2000nM and a maximum potency of 60% of LTD4 [1].

N-Methyll Leukotriene C4 can serve as a fully potent agonist of β - arrestin-2 binding in C2C12 myofibroblasts mediated by the human CysLT2 receptor, with an EC50 of 8.7 nM and a maximum efficacy of up to 90% of LTC4 [1].

N-Methyll Leukotriene C4 (0.4 μg/mL; up to 30 min) was not metabolized by guinea pig lung homogenate, indicating its stability in degradation mediated by gamma glutamyl transpeptidase.

N-Methyll Leukotriene C4 (single push injection, 10 μg) does not metabolize to LTD4 in isolated perfused guinea pig lungs, and its induced perfusion pressure elevation cannot be antagonized by FPL55712.

N-Methyll Leukotriene C4 can induce concentration dependent contraction in the ileum of guinea pigs, with a pD2 value of 7.7.

N-Methyll Leukotriene C4 can induce concentration dependent constriction in guinea pig airways, with a pD2 value of 8.1.

体内研究

N-Methyll Leukotriene C4 (5 ng; intradermal injection; Single dose administration is a potent, CysLT2 receptor selective agonist that can increase vascular permeability by 22 times in transgenic mice overexpressing human CysLT2 receptors in endothelial cells, but has no significant effect on CysLT2 receptor knockout mice [1].
N-Methyll Leukotriene C4 (10-1000 ng/kg bw; intravenous injection; The antihypertensive effect produced by a single injection in the intubated American bullfrog is stronger and lasts longer than that of the natural peptide leukotriene, and its cardiovascular effects are antagonized by high-dose Ablukast at a dose of 100 ng/kg bw or higher [2].
N-Methyll Leukotriene C4 (15-40 μg/kg; intravenous injection) can be used as a weak acting, dose-dependent intravenous bronchoconstrictor in anesthetized guinea pigs, with a potency 25 times lower than LTC4, and its bronchoconstrictive effect can be significantly inhibited by FPL55712 [3].
N-Methyll Leukotriene C4 (20 μg/kg; intravenous injection) can induce significant and persistent pressor effects in anesthetized guinea pigs, which are not significantly affected by LTD4/LTE4 antagonists, lipoxygenase inhibitors, or alpha adrenergic receptor antagonists.

Animal Model:

transgenic mice overexpressing human CysLT₂ receptor in vascular endothelial cells (TG-EC); CysLT₂ receptor knockout (KO) mice

Dosage:

5 ng

Administration:

i.d.; single dose

Result:

Elicited a 22-fold increase in vascular leakage compared with vehicle control in TG-EC mice, with an average absorbance of 0.26 versus 0.012 for vehicle.
Did not produce a statistically significant increase in vascular leakage in CysLT₂ receptor KO mice, with an average absorbance of 0.034 versus 0.063 for vehicle.

Animal Model:	American bullfrog (both sexes, 368.06 g)
Dosage:	10 ng/kg bw; 30 ng/kg bw; 100 ng/kg bw; 300 ng/kg bw; 1000 ng/kg bw
Administration:	i.v.; single bolus
Result:	Exhibited equivalent hypotensive (ΔMAP) potency to LTC₄, LTD₄, and LTE₄ at 10 and 30 ng/kg bw. Produced the most potent hypotensive effect at 100, 300, and 1000 ng/kg bw, with significantly greater ΔMAP reduction than LTC₄, LTD₄, and LTE₄. Induced significantly greater HR responses than LTD₄ and LTE₄ at doses of 100 ng/kg bw and higher. Caused significantly longer duration of cardiovascular effects than LTC₄, LTD₄, and LTE₄ at doses as low as 30 ng/kg bw. Showed significantly reduced MAP and HR responses when co-administered with high-dose Ro 23-3544 at doses of 100 ng/kg bw and higher.

Animal Model:	Dunkin-Hartley (male, 350-450 g, anaesthetised, artificially ventilated, indomethacin pretreatment)
Dosage:	15 μg/kg; 20 μg/kg; 40 μg/kg
Administration:	i.v.
Result:	Produced a dose-dependent increase in total pulmonary resistance (TPR). Increased TPR by ~2% at 15 μg/kg, ~15% at 20 μg/kg, and ~40% at 40 μg/kg. Was approximately 25 times less potent than LTC₄ as an intravenous bronchoconstrictor. Induced a TPR increase of 37% and a mean arterial blood pressure (MAP) increase of 51 mmHg at 20 μg/kg i.v. Reduced the TPR increase by 73% (to 10%) when pretreated with FPL55712 (0.5 mg/kg i.v.), but did not significantly affect the MAP increase.

Animal Model:	Dunkin-Hartley (male, 350-450 g, anaesthetised, artificially ventilated, propranolol pretreatment)
Dosage:	10 μg/mL; 20 μg/mL; 30 μg/mL
Administration:	aerosolised; 20 sec
Result:	Produced a dose-dependent increase in total pulmonary resistance (TPR). Increased TPR by ~28% at 10 μg/mL, ~58% at 20 μg/mL, and ~88% at 30 μg/mL. Was approximately 20 times less potent than LTC₄ as an inhaled bronchoconstrictor. Reduced the TPR response by an average of 91% when pretreated with FPL55712 (0.5 mg/kg i.v.). Reduced the TPR response by 71% when treated with aerosolised LY170680 (0.5 mg/mL for 20 sec). Caused no change in mean arterial blood pressure (MAP).

Animal Model:	Dunkin-Hartley (male, 350-450 g, anaesthetised, artificially ventilated, indomethacin and propranolol pretreatment)
Dosage:	20 μg/kg
Administration:	i.v.
Result:	Induced a mean arterial blood pressure (MAP) increase of 51 mmHg at 20 μg/kg i.v. Showed no significant change in hypertensive effect when pretreated with FPL55712 (0.5 mg/kg i.v.), AA861 (5 mg/kg i.v.), or phenoxybenzamine (1 mg/kg i.v.).

分子式

C₃₁H₄₉N₃O₉S

分子量

639.8

CAS号

131391-65-6

运输条件

Shipping with dry ice.

储存方式

-80°C

纯度： ≥97%

Data Sheet

产品使用指南

[1]. Yan D, et al. Differential signaling of cysteinyl leukotrienes and a novel cysteinyl leukotriene receptor 2 (CysLT₂) agonist, N-methyl-leukotriene C₄, in calcium reporter and β arrestin assays. Mol Pharmacol. 2011 Feb;79(2):270-8.

[2]. Sun J, et al. Cardiovascular effects of N-methyl leukotriene C4, a nonmetabolizable leukotriene C4 analogue, and the antagonism of leukotriene-induced hypotension by Ro 23-3544, in the American bullfrog, Rana catesbeiana. Canadian journal of physiology and pharmacology. 1995 Mar;73(3):383-9.

[3]. Baker SR, et al. The pharmacology of N-methyl LTC4; a metabolically stable LTC4-mimetic. Prostaglandins. 1990 Nov;40(5):445-61.

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动物实验计算换算器