Date published: 2026-5-9

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DHODH Activators

DHODH activators constitute a group of chemical entities that enhance the activity of the enzyme dihydroorotate dehydrogenase, which is intrinsic to the de novo synthesis pathway of pyrimidine nucleotides. These activators can work by a variety of mechanisms, including direct binding to the enzyme to increase its catalytic efficiency, affecting the enzyme's conformation to favor a more active state, or impacting the cellular environment to upregulate the enzyme's expression. The chemical nature of DHODH activators is diverse, encompassing a range of small organic molecules and inorganic compounds that possess the ability to interact with the enzyme or its regulatory pathways. These compounds often have distinct chemical structures, and their influence on DHODH can be the result of specific interactions at the molecular level, which can affect the enzyme's function.

The modulation of DHODH by these activators impacts the production of pyrimidine nucleotides, which are crucial for a variety of cellular processes, including DNA and RNA synthesis. By increasing the activity of DHODH, activators can affect the rate of pyrimidine synthesis. The precise action of these molecules can depend on their structure, the presence of specific functional groups, and their affinity for DHODH or associated cellular components. Moreover, the cellular context plays a significant role in how these activators affect DHODH activity; factors such as the availability of substrates, the presence of other regulatory proteins, and the overall demand for nucleotides within the cell can all influence the outcome of activator interaction. It's important to note that while the alteration of DHODH activity has various consequences on cellular function, the role of these activators is evaluated purely based on their biochemical impact on the enzyme and its associated metabolic pathways.

SEE ALSO...

Product NameCAS #Catalog #QUANTITYPriceCitationsRATING

Leflunomide

75706-12-6sc-202209
sc-202209A
10 mg
50 mg
$20.00
$83.00
5
(1)

Leflunomide metabolite inhibits DHODH activity, which could lead to a compensatory increase in DHODH expression as a feedback mechanism.

Isobavachalcone

20784-50-3sc-202666
1 mg
$213.00
1
(1)

This compound has been reported to inhibit DHODH, potentially triggering a feedback response that increases DHODH expression.

A77 1726

163451-81-8sc-207235
10 mg
$80.00
14
(1)

The active metabolite of leflunomide, known to inhibit DHODH, which may lead to a rise in DHODH expression through feedback mechanisms.

Methotrexate

59-05-2sc-3507
sc-3507A
100 mg
500 mg
$94.00
$213.00
33
(5)

As an antifolate, methotrexate might indirectly increase DHODH expression by causing a demand for nucleotide synthesis through other pathways.

Hydroxyurea

127-07-1sc-29061
sc-29061A
5 g
25 g
$78.00
$260.00
18
(1)

Hydroxyurea inhibits ribonucleotide reductase, which could lead to compensatory upregulation of DHODH as the cell attempts to maintain nucleotide synthesis.

Fluorouracil

51-21-8sc-29060
sc-29060A
1 g
5 g
$37.00
$152.00
11
(1)

As a nucleotide synthesis antagonist, 5-fluorouracil could potentially induce DHODH expression as part of a compensatory cellular response.

Ribavirin

36791-04-5sc-203238
sc-203238A
sc-203238B
10 mg
100 mg
5 g
$63.00
$110.00
$214.00
1
(1)

Ribavirin, a nucleoside analogue, might increase DHODH expression by imposing stress on nucleotide synthesis pathways.

Sulfamethoxazole

723-46-6sc-208405
sc-208405A
sc-208405B
sc-208405C
10 g
25 g
50 g
100 g
$37.00
$55.00
$69.00
$109.00
5
(0)

As a sulfonamide antibiotic, it could indirectly affect nucleotide synthesis, potentially leading to modulation of DHODH expression.

Triacsin C Solution in DMSO

76896-80-5sc-200574
sc-200574A
100 µg
1 mg
$187.00
$843.00
14
(1)

It is known to inhibit long-chain acyl-CoA synthetase, which may influence lipid metabolism and indirectly affect DHODH expression.

β-Pyrazofurin Trifluoroacetic Acid Salt

30868-30-5 (free base)sc-476809
1 mg
$480.00
(0)

Pyrazofurin is known to inhibit orotidine 5'-monophosphate decarboxylase, which could lead to feedback upregulation of DHODH to compensate.