ACOT10 Inhibitors
Chemical inhibitors of acyl-CoA thioesterase 10 can modulate the enzyme's activity by affecting the availability of its substrates or by altering the enzyme's environment in a manner that impacts its function. Triacsin C, for instance, targets the biosynthesis pathway of acyl-CoA by inhibiting long-chain acyl-CoA synthetase. This action diminishes the pool of acyl-CoA molecules, thereby reducing the availability of substrates necessary for acyl-CoA thioesterase 10 to function effectively. Similarly, Perhexiline, Etomoxir, and Oxfenicine obstruct the carnitine palmitoyltransferase-1 (CPT-1), a key transporter of long-chain fatty acids into mitochondria for β-oxidation. These inhibitors lead to an accumulation of long-chain acyl-CoAs, which can saturate acyl-CoA thioesterase 10 to the point of substrate inhibition, impeding its catalytic activity.
Other compounds, such as Malonyl-CoA, interfere with CPT-1 and result in a disruption of the normal acyl-CoA to CoA ratio, which can inhibit acyl-CoA thioesterase 10 activity due to an imbalance in substrate concentration. Mildronate reduces the synthesis of carnitine, thus affecting the transport of fatty acids into the mitochondria and limiting the substrates available for acyl-CoA thioesterase 10, leading to an indirect inhibition of the enzyme. AICAR, by activating AMP-activated protein kinase, can increase fatty acid oxidation, depleting the substrates for acyl-CoA thioesterase 10 and hindering its function. Rimonabant and Nicotinic Acid influence metabolic pathways that lead to reduced synthesis or availability of free fatty acids and their corresponding acyl-CoA derivatives, thereby limiting the substrate for the enzyme. Guggulsterone regulates lipid metabolism, potentially decreasing the synthesis of acyl-CoA molecules and consequently inhibiting acyl-CoA thioesterase 10. Lastly, Fenofibrate and Curcumin can also modulate the activity of acyl-CoA thioesterase 10 by affecting fatty acid β-oxidation and altering lipid metabolism, respectively, which can lead to a reduced pool of acyl-CoA molecules for the enzyme to act upon.
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Items 1 to 10 of 11 total
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Triacsin C Solution in DMSO | 76896-80-5 | sc-200574 sc-200574A | 100 µg 1 mg | $149.00 $826.00 | 14 | |
Triacsin C inhibits long-chain acyl-CoA synthetase, which is responsible for the conversion of free fatty acids into their corresponding acyl-CoA derivatives, a substrate necessary for acyl-CoA thioesterase 10 to catalyze hydrolysis. Inhibition of this upstream enzyme reduces the acyl-CoA pool, leading to functional inhibition of acyl-CoA thioesterase 10 due to substrate scarcity. | ||||||
rac Perhexiline Maleate | 6724-53-4 | sc-460183 | 10 mg | $184.00 | ||
Perhexiline inhibits carnitine palmitoyltransferase-1 (CPT-1), which is crucial for the transport of long-chain fatty acids into mitochondria for β-oxidation. By inhibiting CPT-1, perhexiline leads to an accumulation of long-chain acyl-CoAs, potentially saturating acyl-CoA thioesterase 10 and thus inhibiting its function by substrate inhibition. | ||||||
(+)-Etomoxir sodium salt | 828934-41-4 | sc-215009 sc-215009A | 5 mg 25 mg | $148.00 $496.00 | 3 | |
Etomoxir inhibits the activity of CPT-1, leading to an accumulation of long-chain fatty acyl-CoAs in the cytosol. This accumulation may inhibit acyl-CoA thioesterase 10 by overwhelming the enzyme with excessive substrate, similar to product inhibition. | ||||||
4-Hydroxy-L-phenylglycine | 32462-30-9 | sc-254680A sc-254680 | 5 g 10 g | $82.00 $109.00 | ||
Oxfenicine specifically inhibits CPT-1, which can indirectly lead to an altered acyl-CoA to CoA ratio, thereby inhibiting the activity of acyl-CoA thioesterase 10 due to an imbalance of substrate to product concentrations. | ||||||
Meldonium | 76144-81-5 | sc-207887 | 100 mg | $252.00 | 1 | |
Mildronate inhibits γ-butyrobetaine hydroxylase, which reduces the synthesis of carnitine, a molecule necessary for the transport of fatty acids into the mitochondria. Decreased carnitine levels may lead to an inhibition of acyl-CoA thioesterase 10 by reducing its substrate availability. | ||||||
AICAR | 2627-69-2 | sc-200659 sc-200659A sc-200659B | 50 mg 250 mg 1 g | $60.00 $270.00 $350.00 | 48 | |
AICAR activates AMP-activated protein kinase (AMPK), which can increase fatty acid oxidation and potentially deplete the substrates available for acyl-CoA thioesterase 10, leading to its functional inhibition due to lack of substrate. | ||||||
Rimonabant | 168273-06-1 | sc-205491 sc-205491A | 5 mg 10 mg | $72.00 $160.00 | 15 | |
Rimonabant, by acting as a selective CB1 cannabinoid receptor antagonist, can influence metabolic processes and decrease fatty acid synthesis. This may reduce the availability of acyl-CoA substrates for acyl-CoA thioesterase 10, inhibiting its function. | ||||||
Nicotinic Acid | 59-67-6 | sc-205768 sc-205768A | 250 g 500 g | $61.00 $122.00 | 1 | |
Nicotinic acid inhibits lipolysis in adipose tissue, which can lead to reduced free fatty acid levels in the blood and consequently lower levels of acyl-CoA thioesterase 10 substrates, inhibiting the enzyme's activity. | ||||||
Guggulsterone | 95975-55-6 | sc-203990 sc-203990A | 10 mg 50 mg | $145.00 $615.00 | 1 | |
Guggulsterone has been shown to regulate lipid metabolism, which may lead to reduced synthesis of acyl-CoA molecules, thereby inhibiting acyl-CoA thioesterase 10 activity by limiting substrate availability. | ||||||
Fenofibrate | 49562-28-9 | sc-204751 | 5 g | $40.00 | 9 | |
Fenofibrate activates peroxisome proliferator-activated receptor α (PPARα), leading to increased β-oxidation of fatty acids, which may indirectly inhibit acyl-CoA thioesterase 10 by reducing its acyl-CoA substrates through enhanced degradation. | ||||||