ACSVL5 Inhibitors
The class of ACSVL5 inhibitors encompasses a variety of chemical compounds that intricately modulate the expression and function of Acyl-CoA Synthetase Very Long-Chain Family Member 5 (ACSVL5). Triacsin C stands out as a direct inhibitor, targeting ACSVL5 by disrupting the enzymatic conversion of long-chain fatty acids into acyl-CoA, crucial for lipid metabolism and cellular processes influenced by ACSVL5. This direct inhibition provides a specific mechanism for modulating ACSVL5 expression and function at the enzymatic level. Indirect inhibitors within this class include compounds like Thiazovivin, which inhibits Rho-associated protein kinase (ROCK), leading to modulation of the Rho GTPase signaling pathway indirectly affecting ACSVL5. Similarly, 2-Bromopalmitate, through its action on fatty acid amide hydrolase (FAAH), indirectly influences endocannabinoid signaling, resulting in the modulation of ACSVL5 expression or function. These indirect inhibitors showcase the diverse strategies employed to regulate ACSVL5 through alterations in related cellular pathways.
Moreover, the class includes inhibitors like Etomoxir, targeting carnitine palmitoyltransferase 1 (CPT1) to directly disrupt fatty acid oxidation, providing a precise means of modulating ACSVL5 expression through the inhibition of metabolic processes. Compounds such as PF-543 and H89 act on sphingosine kinase 1 (SphK1) and protein kinase A (PKA), respectively, indirectly influencing ACSVL5 through alterations in downstream signaling pathways associated with sphingolipid metabolism and PKA-dependent processes. In summary, the class of ACSVL5 inhibitors comprises a spectrum of chemical compounds that directly or indirectly modulate cellular pathways associated with ACSVL5. These inhibitors act through well-defined mechanisms, offering a nuanced understanding of how specific biochemical and cellular pathways influence the expression and activity of ACSVL5.
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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 | $187.00 $843.00 | 14 | |
Triacsin C is a potent inhibitor of long-chain acyl-CoA synthetases (ACSVLs). By directly targeting ACSVL5, Triacsin C disrupts the enzymatic conversion of long-chain fatty acids into acyl-CoA, leading to the inhibition of ACSVL5 and its downstream effects on lipid metabolism and cellular processes influenced by ACSVL5. | ||||||
Thiazovivin | 1226056-71-8 | sc-361380 sc-361380A | 10 mg 25 mg | $284.00 $634.00 | 15 | |
Thiazovivin inhibits Rho-associated protein kinase (ROCK), a downstream effector of Rho GTPases. By blocking ROCK, Thiazovivin indirectly modulates the Rho GTPase signaling pathway, which can influence ACSVL5 expression or function. The inhibition of ROCK by Thiazovivin provides an indirect mechanism for modulating ACSVL5 through the regulation of Rho GTPase-dependent pathways. | ||||||
2-Bromohexadecanoic acid | 18263-25-7 | sc-251714 sc-251714A | 10 g 50 g | $53.00 $201.00 | 4 | |
2-Bromohexadecanoic acidis an irreversible inhibitor of fatty acid amide hydrolase (FAAH). By targeting FAAH, 2-Bromopalmitate can indirectly modulate endocannabinoid signaling, affecting ACSVL5 expression or function. This indirect inhibition of ACSVL5 occurs through alterations in the endocannabinoid system and related pathways influenced by FAAH activity. | ||||||
(+)-Etomoxir sodium salt | 828934-41-4 | sc-215009 sc-215009A | 5 mg 25 mg | $151.00 $506.00 | 3 | |
Etomoxir inhibits carnitine palmitoyltransferase 1 (CPT1), a key enzyme involved in fatty acid oxidation. By blocking CPT1, Etomoxir disrupts the metabolic processes associated with ACSVL5, providing a direct means of modulating ACSVL5 expression and function through the inhibition of fatty acid oxidation and the downstream effects on cellular lipid metabolism. | ||||||
PF-543 | 1415562-82-1 | sc-507507 | 10 mg | $210.00 | ||
PF-543 is a selective inhibitor of sphingosine kinase 1 (SphK1). By targeting SphK1, PF-543 modulates sphingolipid metabolism and downstream signaling pathways. This indirect inhibition of ACSVL5 occurs through alterations in sphingolipid levels and related pathways influenced by SphK1 activity, providing a specific mechanism for influencing ACSVL5 expression or function. | ||||||
Sunitinib, Free Base | 557795-19-4 | sc-396319 sc-396319A | 500 mg 5 g | $153.00 $938.00 | 5 | |
Sunitinib is a tyrosine kinase inhibitor that targets multiple receptor tyrosine kinases. By inhibiting these kinases, Sunitinib can indirectly modulate signaling pathways connected to ACSVL5, influencing its expression or function. The indirect inhibition of ACSVL5 by Sunitinib occurs through alterations in tyrosine kinase-dependent pathways, providing a specific mechanism for regulating ACSVL5. | ||||||
BAY 11-7082 | 19542-67-7 | sc-200615B sc-200615 sc-200615A | 5 mg 10 mg 50 mg | $62.00 $85.00 $356.00 | 155 | |
BAY 11-7082 inhibits the activation of NF-κB, a transcription factor involved in inflammatory responses. By modulating NF-κB activity, BAY 11-7082 can indirectly influence ACSVL5 expression, as NF-κB is known to regulate genes involved in the inflammatory signaling cascades linked to ACSVL5 modulation. The inhibition of NF-κB by BAY 11-7082 provides an indirect mechanism for modulating ACSVL5. | ||||||
Rapamycin | 53123-88-9 | sc-3504 sc-3504A sc-3504B | 1 mg 5 mg 25 mg | $63.00 $158.00 $326.00 | 233 | |
Rapamycin inhibits the mechanistic target of rapamycin (mTOR) pathway. By blocking mTOR, Rapamycin can indirectly influence ACSVL5 through the modulation of mTOR-dependent signaling pathways. The inhibition of mTOR by Rapamycin provides an indirect means of modulating ACSVL5 expression or function through alterations in cellular processes governed by mTOR-dependent pathways. | ||||||
GSK 2334470 | 1227911-45-6 | sc-364501 sc-364501A | 10 mg 50 mg | $199.00 $1165.00 | 1 | |
GSK2334470 is a potent inhibitor of RIP3 kinase, a key component of the necroptosis pathway. By blocking RIP3, GSK2334470 can indirectly modulate necroptotic signaling pathways that may intersect with ACSVL5-related pathways. This indirect inhibition of ACSVL5 occurs through alterations in necroptosis-dependent signaling, providing a specific mechanism for influencing ACSVL5 expression or function. | ||||||
Lonidamine | 50264-69-2 | sc-203115 sc-203115A | 5 mg 25 mg | $105.00 $364.00 | 7 | |
Lonidamine disrupts mitochondrial respiration by inhibiting hexokinase II, influencing cellular metabolism. By targeting hexokinase II, Lonidamine can indirectly modulate ACSVL5 through alterations in the glycolytic pathway and related metabolic processes. The inhibition of hexokinase II by Lonidamine provides an indirect means of regulating ACSVL5 expression or function through changes in cellular metabolism. | ||||||