N-Acetylcysteine (NAC chemical, N-Acetyl-L-Cysteine)

製品コードS1623 バッチS162306

化学情報

	Synonyms	N-acetylcysteine	Storage (From the date of receipt)	3 years -20°C powder
	化学式	C₅H₉NO₃S
	分子量	163.19	CAS No.	616-91-1
Solubility (25°C)*	体外	DMSO	33 mg/mL (202.21 mM)
		Water	33 mg/mL (202.21 mM)
		Ethanol	33 mg/mL (202.21 mM)
* <1 mg/ml means slightly soluble or insoluble. * Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

溶剤液（一定の濃度）を調合する

生物活性

製品説明	Acetylcysteine (N-acetyl-l-cysteine, NAC,N-acetylcysteine)は、プロテアソーム阻害剤の活性を阻害するROS（活性酸素種）阻害剤です。また、腫瘍壊死因子産生阻害剤でもあります。Acetylcysteine(N-acetyl-l-cysteine)は、IκBキナーゼの阻害を介してTNF誘導性のNF-κB活性化を抑制します。Acetylcysteine(N-acetyl-l-cysteine)は、ミトコンドリア依存性経路を介してapoptosisを誘導します。Acetylcysteine(N-acetyl-l-cysteine)は、ferroptosisとvirus replicationを阻害します。溶液は不安定なので、新鮮に調製する必要があります。
in vitro	Acetylcysteine (N-Acetylcysteine, NAC) inhibits activation of c-Jun N-terminal kinase, p38 MAP kinase and redox-sensitive activating protein-1 and nuclear factor kappa B transcription factor activities regulating expression of numerous genes. It can also prevent apoptosis and promote cell survival by activating extracellular signal-regulated kinase pathway, a concept useful for treating certain degenerative diseases. This compound directly modifies the activity of several proteins by its reducing activity. It prevents apoptotic DNA fragmentation and maintains long-term survival in the absence of other trophic support in serum-deprived PC12 cells. It also prevents death of PC12 cells and sympathetic neurons. It causes dose-dependent reductions in viability in rat and human aortic smooth muscle cells. It activates the Ras-extracellular signal-regulated kinase (ERK) pathway in PC12 cells. This compound protects neuronal cells from death evoked by withdrawal of trophic support. It increases nitric oxide (NO) release from protein-bound stores in vascular tissue. Its pretreatment of PC12 cells interferes with NGF-dependent signaling and neurite outgrowth, and it was suggested that NAC interferes with redox-sensitive steps in the NGF mechanism.
in vivo	In both the T-maze footshock avoidance paradigm and the lever press appetitive task, N-acetylcysteine (NAC) improves cognition of 12-month-old SAMP8 mice without inducing non-specific effects on motor activity, motivation to avoid shock, or body weight.

製品説明

Acetylcysteine (N-acetyl-l-cysteine, NAC,N-acetylcysteine)は、プロテアソーム阻害剤の活性を阻害するROS（活性酸素種）阻害剤です。また、腫瘍壊死因子産生阻害剤でもあります。Acetylcysteine(N-acetyl-l-cysteine)は、IκBキナーゼの阻害を介してTNF誘導性のNF-κB活性化を抑制します。Acetylcysteine(N-acetyl-l-cysteine)は、ミトコンドリア依存性経路を介してapoptosisを誘導します。Acetylcysteine(N-acetyl-l-cysteine)は、ferroptosisとvirus replicationを阻害します。溶液は不安定なので、新鮮に調製する必要があります。

in vitro

Acetylcysteine (N-Acetylcysteine, NAC) inhibits activation of c-Jun N-terminal kinase, p38 MAP kinase and redox-sensitive activating protein-1 and nuclear factor kappa B transcription factor activities regulating expression of numerous genes. It can also prevent apoptosis and promote cell survival by activating extracellular signal-regulated kinase pathway, a concept useful for treating certain degenerative diseases. This compound directly modifies the activity of several proteins by its reducing activity.

It prevents apoptotic DNA fragmentation and maintains long-term survival in the absence of other trophic support in serum-deprived PC12 cells. It also prevents death of PC12 cells and sympathetic neurons.

It causes dose-dependent reductions in viability in rat and human aortic smooth muscle cells.

It activates the Ras-extracellular signal-regulated kinase (ERK) pathway in PC12 cells. This compound protects neuronal cells from death evoked by withdrawal of trophic support. It increases nitric oxide (NO) release from protein-bound stores in vascular tissue. Its pretreatment of PC12 cells interferes with NGF-dependent signaling and neurite outgrowth, and it was suggested that NAC interferes with redox-sensitive steps in the NGF mechanism.

in vivo

In both the T-maze footshock avoidance paradigm and the lever press appetitive task, N-acetylcysteine (NAC) improves cognition of 12-month-old SAMP8 mice without inducing non-specific effects on motor activity, motivation to avoid shock, or body weight.

プロトコル(参考用のみ)

細胞アッセイ	細胞株	MCF cells
	濃度	5 mM
	反応時間	24 h
	実験の流れ	Cells were treated with the indicated concentration of Acetylcysteine (N-Acetylcysteine, NAC) for 24 h.
動物実験	動物モデル	Male SAMP8 mice
	投薬量	100 mg/kg
	投与方法	s.c.

参考

https://pubmed.ncbi.nlm.nih.gov/11897584/
https://pubmed.ncbi.nlm.nih.gov/7722634/
https://pubmed.ncbi.nlm.nih.gov/8631978/

https://pubmed.ncbi.nlm.nih.gov/9592085/
https://pubmed.ncbi.nlm.nih.gov/12603840/
https://pubmed.ncbi.nlm.nih.gov/23772801/
https://pubmed.ncbi.nlm.nih.gov/1544168/
https://pubmed.ncbi.nlm.nih.gov/29426002/
https://pubmed.ncbi.nlm.nih.gov/30294906/
https://pubmed.ncbi.nlm.nih.gov/35023619/

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カスタマーフィードバック

: Data from [Data independently produced by , , Biochem Pharmacol, 2017, 146:224-232]

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人間や獣医の診断であるか治療的な使用のためにでない。

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