| Candidate ID: | R0264 |
| Source ID: | DB00749 |
| Source Type: | approved; investigational; vet_approved |
| Compound Type: |
small molecule
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| Compound Name: |
Etodolac
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| Synonyms: |
(±)-1,8-diethyl-1,3,4,9-tetrahydropyrano(3,4-b)indole-1-acetic acid; (1,8-Diethyl-1,3,4,9-tetrahydro-pyrano[3,4-b]indol-1-yl)-acetic acid; 1,3,4,9-tetrahydro-1,8-diethylpyrano(3,4-b)indole-1-acetic acid; 1,8-diethyl-1,3,4,9-tetrahydropyrano(3,4-b)indole-1-acetic acid; 1,8-diethyl-1,3,4,9-tetrahydropyrano[3,4-b]indol-1-ylacetic acid; Etodolac; Etodolic acid
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| Molecular Formula: |
C17H21NO3
|
| SMILES: |
CCC1=C2NC3=C(CCOC3(CC)CC(O)=O)C2=CC=C1
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| Structure: |
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| DrugBank Description: |
Etodolac is a non-steroidal anti-inflammatory drug (NSAID) with anti-inflammatory, analgesic and antipyretic properties. Its therapeutic effects are due to its ability to inhibit prostaglandin synthesis. It is indicated for relief of signs and symptoms of rheumatoid arthritis and osteoarthritis.
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| CAS Number: |
41340-25-4
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| Molecular Weight: |
287.3535
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| DrugBank Indication: |
For acute and long-term management of signs and symptoms of osteoarthritis and rheumatoid arthritis, as well as for the management of pain.
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| DrugBank Pharmacology: |
Etodolac is an anti-inflammatory agent with analgesic and antipyretic properties. It is used to treat osteoarthritis, rheumatoid arthritis and control acute pain. The therapeutic effects of etodolac are achieved via inhibition of the synthesis of prostaglandins involved in fever, pain, swelling and inflammation. Etodolac is administered as a racemate. As with other NSAIDs, the S-form has been shown to be active while the R-form is inactive. Both enantiomers are stable and there is no evidence of R- to S- conversion _in vivo_.
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| DrugBank MoA: |
Similar to other NSAIDs, the anti-inflammatory effects of etodolac result from inhibition of the enzyme cycooxygenase (COX). This decreases the synthesis of peripheral prostaglandins involved in mediating inflammation. Etodolac binds to the upper portion of the COX enzyme active site and prevents its substrate, arachidonic acid, from entering the active site. Etodolac was previously thought to be a non-selective COX inhibitor, but it is now known to be 5 – 50 times more selective for COX-2 than COX-1. Antipyresis may occur by central action on the hypothalamus, resulting in peripheral dilation, increased cutaneous blood flow, and subsequent heat loss.
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| Targets: |
Prostaglandin G/H synthase 2 inhibitor; Prostaglandin G/H synthase 1 inhibitor; Retinoic acid receptor RXR-alpha other
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| Inclusion Criteria: |
Therapeutic strategy associated
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