| Candidate ID: | R0281 |
| Source ID: | DB00788 |
| Source Type: | approved; vet_approved |
| Compound Type: |
small molecule
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| Compound Name: |
Naproxen
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| Synonyms: |
(+)-(S)-6-Methoxy-α-methyl-2-naphthaleneacetic acid; (+)-(S)-Naproxen; (+)-2-(6-Methoxy-2-naphthyl)propionic acid; (+)-2-(Methoxy-2-naphthyl)-propionic acid; (+)-Naproxen; (S)-(+)-2-(6-Methoxy-2-naphthyl)propionic acid; (S)-(+)-Naproxen; (S)-2-(6-Methoxy-2-naphthyl)propanoic acid; (S)-2-(6-Methoxy-2-naphthyl)propionic acid; (S)-6-Methoxy-alpha-methyl-2-naphthaleneacetic acid; (S)-Naproxen; Naprolag
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| Molecular Formula: |
C14H14O3
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| SMILES: |
COC1=CC2=C(C=C1)C=C(C=C2)[C@H](C)C(O)=O
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| Structure: |
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| DrugBank Description: |
Naproxen is classified as a nonsteroidal anti-inflammatory dug (NSAID) and was initially approved for prescription use in 1976 and then for over-the-counter (OTC) use in 1994. It can effectively manage acute pain as well as pain related to rheumatic diseases, and has a well studied adverse effect profile. Given its overall tolerability and effectiveness, naproxen can be considered a first line treatment for a variety of clinical situations requiring analgesia. Naproxen is available in both immediate and delayed release formulations, in combination with sumatriptan to treat migraines, and in combination with esomeprazole to lower the risk of developing gastric ulcers.
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| CAS Number: |
22204-53-1
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| Molecular Weight: |
230.2592
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| DrugBank Indication: |
Naproxen is indicated for the management of rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, polyarticular juvenile idiopathic arthritis, tendinitis, bursitis, acute gout, primary dysmenorrhea, and for the relief of mild to moderate pain. Further, it is first-line therapy for osteoarthritis, acute gouty arthritis, dysmenorrhea, and musculoskeletal inflammation and pain.
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| DrugBank Pharmacology: |
Naproxen is an established non-selective NSAID and is useful as an analgesic, anti-inflammatory and antipyretic. Similar to other NSAIDs, the pharmacological activity of naproxen can be attributed to the inhibition of cyclo-oxygenase, which in turn reduces prostaglandin synthesis in various tissues and fluids including the synovial fluid, gastric mucosa, and the blood.
Although naproxen is an effective analgesic, it can have unintended deleterious effects in the patient. For instance, naproxen can adversely affect blood pressure control. A study found that use of naproxen induced an increase in blood pressure, although the increase was not as significant as that found with ibuprofen use.
Further, studies have found that the risk of upper gastrointestinal bleeding is on average four-fold higher for individuals taking NSAIDs. Other factors that increase the risk of upper gastrointestinal bleeding include concurrent use of corticosteroids or anticoagulants, and a history of gastrointestinal ulcers.
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| DrugBank MoA: |
As with other non-selective NSAIDs, naproxen exerts it's clinical effects by blocking COX-1 and COX-2 enzymes leading to decreased prostaglandin synthesis. Although both enzymes contribute to prostaglandin production, they have unique functional differences. The COX-1 enzymes is constitutively active and can be found in normal tissues such as the stomach lining, while the COX-2 enzyme is inducible and produces prostaglandins that mediate pain, fever and inflammation. The COX-2 enzyme mediates the desired antipyretic, analgesic and anti-inflammatory properties offered by Naproxen, while undesired adverse effects such as gastrointestinal upset and renal toxicities are linked to the COX-1 enzyme.
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| Targets: |
Prostaglandin G/H synthase 1 inhibitor; Peptostreptococcal albumin-binding protein; Prostaglandin G/H synthase 2 inhibitor
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| Inclusion Criteria: |
Therapeutic strategy associated
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