Pain Killer Rofecoxib White Raw Powder Analgesic - Antipyretic CAS 162011-90-7

Pain Killer Rofecoxib CAS: 162011-90-7 Raw Powder Analgesic-Antipyretic

Description:

Rofecoxib is used for the treatment of osteoarthritis, rheumatoid arthritis, acute pain in adults, and primary dysmenorrhea, as well as acute treatment of migraine attacks with or without auras. Rofecoxib is a solid. This compound belongs to the stilbenes. These are organic compounds containing a 1,2-diphenylethylene moiety. Stilbenes (C6-C2-C6 ) are derived from the common phenylpropene (C6-C3) skeleton building block. The introduction of one or more hydroxyl groups to a phenyl ring lead to stilbenoids. Rofecoxib has a half-life of 17 hours and its mean oral bioavailability at therapeutically recommended doses of 125, 25, and 50 mg is approximately 93%. The proteins that rofecoxib target include elastin and prostaglandin G/H synthase 2. Cytochrome P450 1A2, Cytochrome P450 3A4, Cytochrome P450 2C9, Cytochrome P450 2C8, and Prostaglandin G/H synthase 1 are known to metabolize rofecoxib. On September 30, 2004, Merck voluntarily withdrew rofecoxib from the market because of concerns about increased risk of heart attack and stroke associated with long-term, high-dosage use.

Basic information:

Chemical name: Rofecoxib
Other names: Rofecoxib; 162011-90-7; Vioxx; Ceoxx; MK 966; 4-[4-(methylsulfonyl)phenyl]-3-phenylfuran-2(5H)-one
MF: C17H14O4S
MW: 314.36
CAS: 162011-90-7
Appearance: White powder
Purity: over 99%

COA:

BACKGROUND:

The NSAID rofecoxib is a selective cyclooxygenase-2 (COX-2) inhibitor. Its anti-inflammatory and analgesic effects appear to result from the inhibition of prostaglandin synthesis. In 2004, Merck voluntarily withdrew rofecoxib amid controversy over cardiovascular side effects.

In Alzheimers research, interest in NSAIDs arose when epidemiological studies started reporting lower rates of Alzheimers disease or protection of cognition among people who had been taking these drugs for chronic treatment of inflammatory conditions (e.g., Mar 1997 news story; in Veld et al., 1998; Nov 2001 news story; Vlad et al., 2008; Obermann et al., 2013). Experimental studies supported the argument that inflammation plays a role in Alzheimers pathogenesis, prompting a wave of clinical trials of various NSAIDs, such as ibuprofen, naproxen celecoxib, and R-flurbiprofen.

Mode of action:

Cyclooxygenase (COX) has two well-studied isoforms, called COX-1 and COX-2. COX-1 mediates the synthesis of prostaglandins responsible for protection of the stomach lining, while COX-2 mediates the synthesis of prostaglandins responsible for pain and inflammation. By creating "selective" NSAIDs that inhibit COX-2, but not COX-1, the same pain relief as traditional NSAIDs is offered, but with greatly reduced risk of fatal or debilitating peptic ulcers. Rofecoxib is a selective COX-2 inhibitor, or "coxib".

Others include Mercks etoricoxib (Arcoxia), Pfizer’s celecoxib (Celebrex) and valdecoxib (Bextra). Interestingly, at the time of its withdrawal, rofecoxib was the only coxib with clinical evidence of its superior gastrointestinal adverse effect profile over conventional NSAIDs. This was largely based on the VIGOR. study, which compared the efficacy and adverse effect profiles of rofecoxib and naproxen.

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