AKR1C20 Inhibitors
Chemical inhibitors of AKR1C20 can impede the protein's function by reducing the availability of its substrates, prostaglandins. Flufenamic acid, a fenamate group nonsteroidal anti-inflammatory drug (NSAID), can inhibit the protein by limiting the synthesis of prostaglandins via the inhibition of prostaglandin synthetase. Similarly, indomethacin, by inhibiting cyclooxygenase (COX), can decrease prostaglandin production and thus indirectly inhibit AKR1C20. Sulindac, through its active metabolites, inhibits both COX-1 and COX-2 enzymes, leading to a decrease in prostaglandin synthesis and a subsequent reduction in AKR1C20 activity due to a lack of substrate. Aspirin, which irreversibly inhibits COX enzymes, also results in decreased prostaglandin synthesis, further inhibiting AKR1C20 activity indirectly.
Continuing with the theme of COX inhibition, ibuprofen and naproxen both inhibit COX enzymes, which leads to reduced prostaglandin synthesis and thus a decrease in AKR1C20 activity. Ketoprofen adds to this list by similarly decreasing the synthesis of prostaglandins and therefore inhibiting AKR1C20. Piroxicam inhibits prostaglandin synthesis by blocking COX enzymes, again resulting in decreased AKR1C20 activity. Mefenamic acid, another fenamate group NSAID, inhibits COX and reduces prostaglandin synthesis, indirectly inhibiting AKR1C20. Diclofenac, known for potent COX inhibition, reduces prostaglandin synthesis and subsequently inhibits AKR1C20. Celecoxib, a selective COX-2 inhibitor, also reduces prostaglandin levels, inhibiting AKR1C20. Lastly, acetaminophen, primarily affecting COX-2 in the brain, reduces the synthesis of prostaglandins, thus limiting the activity of AKR1C20. All these chemicals share a common mechanism of reducing prostaglandin synthesis, which is crucial for AKR1C20 activity, thereby inhibiting the protein's function by decreasing the availability of its substrates.
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Items 1 to 10 of 11 total
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Flufenamic acid | 530-78-9 | sc-205699 sc-205699A sc-205699B sc-205699C | 10 g 50 g 100 g 250 g | $27.00 $79.00 $154.00 $309.00 | 1 | |
Flufenamic acid, a member of the fenamate group of nonsteroidal anti-inflammatory drugs, is known to inhibit prostaglandin synthetase. AKR1C20 is implicated in prostaglandin metabolism. The inhibition of prostaglandin synthetase can reduce the substrate availability for AKR1C20. | ||||||
Indomethacin | 53-86-1 | sc-200503 sc-200503A | 1 g 5 g | $29.00 $38.00 | 18 | |
Indomethacin acts as a cyclooxygenase (COX) inhibitor. By inhibiting COX, the production of prostaglandins is reduced. AKR1C20 is involved in the reduction of prostaglandins, thus indomethacin's action can decrease the functional requirement of AKR1C20. | ||||||
Sulindac | 38194-50-2 | sc-202823 sc-202823A sc-202823B | 1 g 5 g 10 g | $32.00 $86.00 $150.00 | 3 | |
Sulindac, through its metabolites, inhibits COX-1 and COX-2, leading to decreased synthesis of prostaglandins. AKR1C20, which plays a role in reducing prostaglandins, would have reduced substrate to act upon, thereby inhibiting its function. | ||||||
Aspirin | 50-78-2 | sc-202471 sc-202471A | 5 g 50 g | $20.00 $42.00 | 4 | |
Aspirin irreversibly inhibits COX enzymes, which are involved in the production of prostaglandins. With reduced prostaglandin synthesis, the activity of AKR1C20, which reduces prostaglandins, would be indirectly inhibited due to lack of substrate. | ||||||
Ibuprofen | 15687-27-1 | sc-200534 sc-200534A | 1 g 5 g | $53.00 $88.00 | 6 | |
Ibuprofen is a COX inhibitor that leads to decreased prostaglandin synthesis. With prostaglandin levels lowered, AKR1C20's role in their reduction is inhibited as the availability of its substrates is decreased. | ||||||
Naproxen | 22204-53-1 | sc-200506 sc-200506A | 1 g 5 g | $24.00 $41.00 | ||
Naproxen inhibits both COX-1 and COX-2, reducing prostaglandin synthesis. Since AKR1C20 is involved in prostaglandin metabolism, naproxen's action indirectly inhibits AKR1C20 activity by limiting its substrate. | ||||||
Ketoprofen | 22071-15-4 | sc-205359 sc-205359A | 5 g 25 g | $126.00 $339.00 | 2 | |
Ketoprofen is a COX inhibitor, decreasing the synthesis of prostaglandins. AKR1C20, which participates in the prostaglandin metabolic pathway, would be functionally inhibited as the availability of prostaglandins is reduced. | ||||||
Piroxicam | 36322-90-4 | sc-200576 sc-200576A | 1 g 5 g | $109.00 $376.00 | 2 | |
Piroxicam inhibits prostaglandin synthesis by blocking COX enzymes. This action results in decreased substrate for AKR1C20, which is involved in the reduction of prostaglandins, thus inhibiting its activity. | ||||||
Mefenamic acid | 61-68-7 | sc-205380 sc-205380A | 25 g 100 g | $106.00 $208.00 | 6 | |
Mefenamic acid is part of the fenamate group and acts as a COX inhibitor. It reduces prostaglandin synthesis, and thus, indirectly inhibits the function of AKR1C20 by reducing the availability of prostaglandins for reduction. | ||||||
Diclofenac acid | 15307-86-5 | sc-357332 sc-357332A | 5 g 25 g | $109.00 $298.00 | 5 | |
Diclofenac is known for its potent COX inhibition, leading to reduced prostaglandin synthesis. AKR1C20's function is inhibited as the production of prostaglandins, its substrates, is decreased. | ||||||