GNPAT Inhibitors
Chemical inhibitors of GNPAT can exert their inhibitory effects through various mechanisms that impact the ether lipid biosynthesis pathway. Peroxisome proliferators, such as gemfibrozil, induce the proliferation of peroxisomes, which in turn upregulates peroxisomal β-oxidation. This process can deplete the levels of fatty acids available for GNPAT to use in ether lipid synthesis. Tamoxifen, known to disrupt lipid metabolism, can cause an imbalance in lipid synthesis and storage, thereby reducing the substrate availability crucial for GNPAT's enzymatic activity. Similarly, phthalates, especially di-(2-ethylhexyl) phthalate, disrupt lipid metabolism, which can decrease the availability of lipid substrates GNPAT needs for its function.
Triacsin C, an inhibitor of long-chain acyl-CoA synthetase, decreases the acyl-CoA pool necessary for GNPAT activity by preventing the activation of fatty acids. In the same vein, cerulenin, by inhibiting fatty acid synthase, limits the synthesis of fatty acids, thus reducing the precursors needed for GNPAT-mediated ether lipid synthesis. Etomoxir, a carnitine palmitoyltransferase 1 (CPT1) inhibitor, can lead to increased fatty acyl-CoA levels, which can result in product inhibition of GNPAT. Chlorpromazine and thioridazine, both affecting lipid metabolism, can decrease the availability of substrates for GNPAT, thereby functionally inhibiting its role in synthesizing ether lipids. Triclosan, an antimicrobial agent, inhibits fatty acid synthesis, which can lead to a reduction in substrate availability for GNPAT. Statins, including lovastatin, simvastatin, and atorvastatin, inhibit HMG-CoA reductase and are known to affect cholesterol and lipid synthesis pathways. The inhibition of HMG-CoA reductase by these statins can lead to a complex alteration in cellular lipid profiles, which can reduce the pool of lipid substrates that GNPAT requires. This reduction in substrate availability can functionally inhibit the activity of GNPAT in the synthesis of ether lipids.
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Items 1 to 10 of 11 total
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Gemfibrozil | 25812-30-0 | sc-204764 sc-204764A | 5 g 25 g | $66.00 $267.00 | 2 | |
Peroxisome proliferators such as fibric acid derivatives can lead to the proliferation of peroxisomes in cells, increasing the degradation of fatty acids. Since GNPAT (Dihydroxyacetone phosphate acyltransferase) is involved in the ether lipid biosynthesis pathway which takes place in peroxisomes, the upregulation of peroxisomal β-oxidation can reduce the availability of fatty acids for ether lipid synthesis, thus functionally inhibiting the activity of GNPAT. | ||||||
Tamoxifen | 10540-29-1 | sc-208414 | 2.5 g | $272.00 | 18 | |
Tamoxifen has been shown to alter lipid metabolism and can induce lipid droplet accumulation. By disrupting the balance of lipid synthesis and storage, tamoxifen can indirectly affect the substrate availability for GNPAT, which requires acyl-CoA substrates for the synthesis of alkyl glycerolipids. | ||||||
Triacsin C Solution in DMSO | 76896-80-5 | sc-200574 sc-200574A | 100 µg 1 mg | $187.00 $843.00 | 14 | |
Triacsin C is an inhibitor of long-chain acyl-CoA synthetase, which is required for the activation of fatty acids to acyl-CoA, a substrate for the ether lipid synthesis pathway. Inhibition of acyl-CoA synthetase would decrease the acyl-CoA pool, thus functionally inhibiting GNPAT. | ||||||
Cerulenin (synthetic) | 17397-89-6 | sc-200827 sc-200827A sc-200827B | 5 mg 10 mg 50 mg | $161.00 $312.00 $1210.00 | 9 | |
Cerulenin is an inhibitor of fatty acid synthase, which is essential for the synthesis of fatty acids. By inhibiting fatty acid synthesis, cerulenin can decrease the availability of fatty acid substrates for the synthesis of acyl-CoA and subsequently ether lipids, thereby inhibiting GNPAT. | ||||||
(+)-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), leading to reduced fatty acid oxidation. This inhibition can increase fatty acyl-CoA levels within the cell, which could inhibit GNPAT by product inhibition, as GNPAT uses acyl-CoA as a substrate. | ||||||
Thioridazine Hydrochloride | 130-61-0 | sc-201149A sc-201149 sc-201149B sc-201149C sc-201149D | 5 mg 1 g 5 g 25 g 100 g | $20.00 $49.00 $104.00 $416.00 $1248.00 | ||
Thioridazine has been shown to disrupt various lipid metabolism processes. Although not a direct inhibitor, its impact on lipid synthesis and remodeling can reduce the availability of lipid substrates required by GNPAT for ether lipid synthesis. | ||||||
Chlorpromazine | 50-53-3 | sc-357313 sc-357313A | 5 g 25 g | $61.00 $110.00 | 21 | |
Chlorpromazine can alter cellular lipid metabolism and has been reported to affect membrane lipid composition. This alteration might decrease the substrate availability for GNPAT, functionally inhibiting its activity in ether lipid synthesis. | ||||||
Triclosan | 3380-34-5 | sc-220326 sc-220326A | 10 g 100 g | $141.00 $408.00 | ||
Triclosan affects lipid synthesis by inhibiting fatty acid synthesis. This reduction in fatty acid availability can limit the substrate pool for acyl-CoA, subsequently inhibiting GNPAT's ability to synthesize ether lipids. | ||||||
Lovastatin | 75330-75-5 | sc-200850 sc-200850A sc-200850B | 5 mg 25 mg 100 mg | $29.00 $90.00 $339.00 | 12 | |
Lovastatin inhibits HMG-CoA reductase, which is crucial for cholesterol synthesis. This inhibition can have pleiotropic effects on lipid metabolism, potentially reducing the availability of substrates necessary for GNPAT function. | ||||||
Simvastatin | 79902-63-9 | sc-200829 sc-200829A sc-200829B sc-200829C | 50 mg 250 mg 1 g 5 g | $31.00 $89.00 $135.00 $443.00 | 13 | |
Simvastatin, similar to lovastatin, inhibits HMG-CoA reductase, leading to altered lipid profiles and potentially disrupting the lipid substrate availability for ether lipid synthesis, thus indirectly inhibiting GNPAT. | ||||||