Chemical inhibitors of peroxisomal enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase (PECR) can act through indirect mechanisms by modulating lipid metabolism pathways. Fenofibrate, gemfibrozil, WY-14643, and clofibrate are all agonists of peroxisome proliferator-activated receptor alpha (PPARα). Activation of PPARα leads to the upregulation of genes involved in peroxisomal proliferation and fatty acid oxidation. This increased beta-oxidation of fatty acids within the peroxisomes can lead to a reduction in the availability of PECR substrates. By catalyzing the beta-oxidation of fatty acids, these chemicals essentially reduce the pool of fatty acids that PECR would typically modify, indirectly inhibiting the enzyme's activity within its usual metabolic context.
Other chemical inhibitors influence PECR through different pathways related to lipid metabolism. GSK3787, as a PPARδ antagonist, and GW9662 and BADGE, both PPARγ antagonists, alter the lipid metabolic pathways, which can change the availability of substrates or cofactors necessary for PECR activity. By blocking these receptors, these chemicals can affect the balance of lipid synthesis and breakdown, which can reduce the efficacy of PECR's role in processing fatty acids. On another front, MK886, PD146176, nordihydroguaiaretic acid, esculetin, and zileuton act as inhibitors of various lipoxygenase enzymes, which are key in the metabolism of inflammatory lipid mediators. By inhibiting these pathways, these chemicals can change the cellular lipid profile and signaling, which in turn can lead to an indirect inhibition of PECR by shifting the equilibrium of fatty acid metabolism away from the pathways in which PECR is involved.
| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Fenofibrate | 49562-28-9 | sc-204751 | 5 g | $41.00 | 9 | |
Fenofibrate activates peroxisome proliferator-activated receptor alpha (PPARα). PECR is involved in fatty acid metabolism and peroxisomal function. Activation of PPARα signaling can lead to upregulation of peroxisomal proliferation and fatty acid oxidation, which can indirectly inhibit PECR by reducing substrate availability and altering the lipid metabolism equilibrium. | ||||||
Gemfibrozil | 25812-30-0 | sc-204764 sc-204764A | 5 g 25 g | $66.00 $267.00 | 2 | |
Gemfibrozil is another PPARα agonist, which similarly to fenofibrate, can lead to increased fatty acid oxidation. By enhancing the beta-oxidation of fatty acids, gemfibrozil indirectly decreases the availability of PECR substrates and inhibits its function as part of fatty acid metabolism. | ||||||
WY 14643 | 50892-23-4 | sc-203314 | 50 mg | $136.00 | 7 | |
WY-14643 is a potent PPARα agonist that can lead to an indirect inhibition of PECR by promoting peroxisomal proliferation and beta-oxidation, thus reducing the pool of fatty acids available for PECR's enzymatic activity. | ||||||
Clofibrate | 637-07-0 | sc-200721 | 1 g | $33.00 | ||
Clofibrate, yet another PPARα agonist, can lead to the indirect inhibition of PECR by enhancing the peroxisomal beta-oxidation pathway, which limits the substrate required for PECR's activity in fatty acid metabolism. | ||||||
GW 9662 | 22978-25-2 | sc-202641 | 5 mg | $70.00 | 30 | |
GW9662 is a PPARγ antagonist. It could indirectly inhibit PECR by altering lipid metabolism and energy homeostasis within the cell, potentially reducing the availability of substrates or cofactors that PECR requires for its activity. | ||||||
BADGE | 1675-54-3 | sc-202487 sc-202487A sc-202487B sc-202487C | 25 g 50 g 100 g 500 g | $39.00 $51.00 $64.00 $193.00 | 3 | |
Bisphenol A diglycidyl ether (BADGE) is a PPARγ antagonist. By inhibiting PPARγ, BADGE can influence the overall lipid metabolism, potentially reducing the efficacy of PECR's role in fatty acid metabolism due to changes in the metabolic environment. | ||||||
MK-886 sodium salt | 118427-55-7 | sc-200608B sc-200608 sc-200608A | 1 mg 5 mg 25 mg | $47.00 $95.00 $378.00 | 3 | |
MK886 is an inhibitor of 5-lipoxygenase-activating protein (FLAP), which can indirectly inhibit PECR by altering leukotriene synthesis and thus impacting inflammatory processes that may affect cellular lipid metabolism, leading to changes in the cellular environment that are less conducive to PECR's activity. | ||||||
NDGA (Nordihydroguaiaretic acid) | 500-38-9 | sc-200487 sc-200487A sc-200487B | 1 g 5 g 25 g | $109.00 $384.00 $2190.00 | 3 | |
Nordihydroguaiaretic acid is a lipoxygenase inhibitor and may indirectly inhibit PECR by affecting the metabolism of lipids, particularly those involved in inflammatory responses, which could alter the cellular metabolic state and reduce PECR activity. | ||||||
Esculetin | 305-01-1 | sc-200486 sc-200486A | 1 g 5 g | $44.00 $212.00 | 7 | |
Esculetin is a coumarin derivative that inhibits lipoxygenase enzymes. Through the inhibition of these enzymes, it can affect lipid metabolism and signaling, leading to an indirect inhibition of PECR by potentially reducing the availability of its substrates within the cellular lipid metabolism pathways. | ||||||
Zileuton | 111406-87-2 | sc-204417 sc-204417A sc-204417B sc-204417C | 10 mg 50 mg 1 g 75 g | $84.00 $307.00 $369.00 $1254.00 | 8 | |
Zileuton is a selective 5-lipoxygenase inhibitor, which by reducing leukotriene production can alter inflammatory processes and lipid signaling, indirectly inhibiting PECR by influencing the cellular context in which PECR operates, particularly regarding the metabolism of fatty acids. | ||||||