1. NF-κB Anti-infection Metabolic Enzyme/Protease Apoptosis
  2. NF-κB HIV Mitochondrial Metabolism Endogenous Metabolite Apoptosis
  3. α-Lipoic Acid sodium

α-Lipoic Acid sodium  (Synonyms: Thioctic acid sodium; (±)-α-Lipoic acid sodium; DL-α-Lipoic acid sodium)

Cat. No.: HY-N0492A
Handling Instructions

α-Lipoic Acid (Thioctic acid) sodium is an antioxidant, which is an essential cofactor of mitochondrial enzyme complexes. α-Lipoic Acid sodium inhibits NF-κB-dependent HIV-1 LTR activation. α-Lipoic Acid sodium induces endoplasmic reticulum (ER) stress-mediated apoptosis in hepatoma cells. α-Lipoic Acid sodium can be used with CPUL1 (HY-151802) to construct the self-assembled nanoaggregate CPUL1-LA NA, which has improved antitumor efficacy than CPUL1.

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α-Lipoic Acid sodium Chemical Structure

α-Lipoic Acid sodium Chemical Structure

CAS No. : 2319-84-8

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Description

α-Lipoic Acid (Thioctic acid) sodium is an antioxidant, which is an essential cofactor of mitochondrial enzyme complexes. α-Lipoic Acid sodium inhibits NF-κB-dependent HIV-1 LTR activation[1][2][3]. α-Lipoic Acid sodium induces endoplasmic reticulum (ER) stress-mediated apoptosis in hepatoma cells[4]. α-Lipoic Acid sodium can be used with CPUL1 (HY-151802) to construct the self-assembled nanoaggregate CPUL1-LA NA, which has improved antitumor efficacy than CPUL1[5].

IC50 & Target

HIV-1

 

NF-κB

 

Human Endogenous Metabolite

 

Microbial Metabolite

 

In Vitro

The long terminal repeat (LTR) of HIV-1 is the target of cellular transcription factors such as NF-κB, and serves as the promoter-enhancer for the viral genome when integrated in host DNA[1]. α-Lipoic Acid (Alpha-Lipoic acid, ALA), a naturally occurring dithiol compound, plays an essential role in mitochondrial bioenergetics. α-Lipoic Acid reduces lipid accumulation in the liver by regulating the transcriptional factors SREBP-1, FoxO1, and Nrf2, and their downstream lipogenic targets via the activation of the SIRT1/LKB1/AMPK pathway. Treatment of cells with α-Lipoic Acid (250, 500 and 1000 μM) significantly increases the NAD+/NADH ratio in HepG2 cells (P<0.05 or P<0.01). Treatment with α-Lipoic Acid (50, 125, 250 and 500 μM) increases SIRT1 activity in HepG2 cells. α-Lipoic Acid (50, 125, 250, 500 and 1000 μM) increases phosphorylation of AMPK and acetyl-CoA carboxylase (ACC) in HepG2 cells in a dose-dependent fashion[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

C57BL/6J mice, divided into four groups, are fed an high-fat diet (HFD) for 24 weeks to induce nonalcoholic fatty liver disease (NAFLD) followed by daily administration of α-Lipoic Acid. Then, the effects of α-Lipoic Acid on hepatic lipid accumulation in long-term HFD-fed mice are assessed. Administration of α-Lipoic Acid (100 mg/kg or 200 mg/kg) markedly reduces visceral fat mass in mice. In addition, α-Lipoic Acid (100 mg/kg or 200 mg/kg) treatment inhibits the appetite and causes a dramatic weight loss (all P<0.05)[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Clinical Trial
Molecular Weight

228.31

Formula

C8H13NaO2S2

CAS No.
SMILES

O=C(O[Na])CCCCC1SSCC1

Structure Classification
Initial Source
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Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

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    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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α-Lipoic Acid sodium
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HY-N0492A
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