DDInter1729 DDInter1725
Sulindac is a nonsteroidal anti-inflammatory drug (NSAID) of the arylalkanoic acid class that is marketed by Merck under the brand name Clinoril. Like other NSAIDs, it may be used in the treatment of acute or chronic inflammatory conditions. Sulindac is a prodrug, derived from sulfinylindene, that is converted _in vivo_ to an active sulfide compound by liver enzymes. There is evidence from some studies that sulindac may be associated with fewer gastrointestinal side effects than other NSAIDs, except for the cyclooxygenase-2 (COX-2) inhibitor drug class. This may be due to the sulfide metabolite undergoing enterohepatic circulation thus maintaining constant blood levels of the compound without inducing gastrointestinal effects, where the drug is excreted in the bile and then reabsorbed from the intestines. While its full mechanism of action is not fully understood, sulindac
Sulfasalazine is an anti-inflammatory drug structurally related to salicylates and other non-steroidal anti-inflammatory drugs. It is indicated for managing inflammatory diseases such as ulcerative colitis and rheumatoid arthritis (RA).[L39065, A255582] Metabolized by intestinal bacteria, sulfasalazine is broken down into [mesalazine] and [sulfapyridine], 2 compounds that carry out the main pharmacological activity of sulfasalazine. Sulfasalazine was first used in 1940 for rheumatic polyarthritis, and has been firmly established itself as one fo the most useful disease-modifying antirheumatic drug (DMARD). Compared to the first line treatment of RA like methotrexate, sulfasalazine is almost as efficacious as methotrexate although with slightly less tolerability. However, sulfasalazine has less teratogenic side effects and faster onset of action compared to conventional DMARD. Sulfasalazine fell out of favor as the drug of choice for RA due to poorly designed clinical trials in 1950 but regained interest from the clinical community in the late 1970. Although sulfasalazine is only approved by the FDA for ulcerative colitis, research have shown that sulfasalazine is also beneficial for patients with Crohn's disease. Meta-analysis of 19 randomized controlled trials indicated that sulfasalazine is superior to placebo in inducing remission; however, with no supported evidence of mucosal healing, sulfasalazine is not FDA-recommmended for treatment of Crohn's disease.[A255597,A255602,A255607]
Sulindac {u} (Compound) binds {v} (Gene) PTGS1
PTGS1 {u} (Gene) is bound by {v} (Compound) Sulfasalazine
Sulindac {u} (Compound) binds {v} (Gene) PTGS2
PTGS2 {u} (Gene) is bound by {v} (Compound) and {u} (Gene) is upregulated by {v} (Compound) Sulfasalazine
Sulindac {u} (Compound) binds {v} (Gene) PTGS1
PTGS1 {u} (Gene) is bound by {v} (Compound) Olsalazine
Olsalazine {u} (Compound) resembles {v} (Compound) Sulfasalazine
Sulindac {u} (Compound) binds {v} (Gene) CYP1A2
CYP1A2 {u} (Gene) is bound by {v} (Compound) Methoxyflurane
Methoxyflurane {u} may cause a moderate interaction that could exacerbate diseases when taken with {v} Sulfasalazine
Sulindac {u} (Compound) binds {v} (Gene) PTGS1
PTGS1 {u} (Gene) is bound by {v} (Compound) Balsalazide
Balsalazide {u} (Compound) resembles {v} (Compound) Sulfasalazine
Sulindac {u} (Compound) binds {v} (Gene) PTGDR2
PTGDR2 {u} (Gene) is bound by {v} (Compound) Indomethacin
Indomethacin {u} may cause a moderate interaction that could exacerbate diseases when taken with {v} Sulfasalazine
Sulindac {u} (Compound) binds {v} (Gene) CYP1A2
CYP1A2 {u} (Gene) is bound by {v} (Compound) Phenobarbital
Phenobarbital {u} may cause a minor interaction that can limit clinical effects when taken with {v} Sulfasalazine
Sulindac {u} (Compound) binds {v} (Gene) PTGS1
PTGS1 {u} (Gene) is associated with {v} (Disease) ulcerative colitis
ulcerative colitis {u} (Disease) is treated by {v} (Compound) Sulfasalazine
Sulindac {u} (Compound) binds {v} (Gene) AKR1B1
AKR1B1 {u} (Gene) regulates {v} (Gene) ACAT1
ACAT1 {u} (Gene) is bound by {v} (Compound) Sulfasalazine
Sulindac {u} (Compound) binds {v} (Gene) AKR1B1
AKR1B1 {u} (Gene) regulates {v} (Gene) UBQLN2
UBQLN2 {u} (Gene) is downregulated by {v} (Compound) Sulfasalazine
Sulindac (Compound) binds PTGS1 (Gene) and PTGS1 (Gene) is bound by Sulfasalazine (Compound)
Sulindac (Compound) binds PTGS2 (Gene) and PTGS2 (Gene) is bound by Sulfasalazine (Compound) and PTGS2 (Gene) is upregulated by Sulfasalazine (Compound)
Sulindac (Compound) binds PTGS1 (Gene) and PTGS1 (Gene) is bound by Olsalazine (Compound) and Olsalazine (Compound) resembles Sulfasalazine (Compound)
Sulindac (Compound) binds CYP1A2 (Gene) and CYP1A2 (Gene) is bound by Methoxyflurane (Compound) and Methoxyflurane may cause a moderate interaction that could exacerbate diseases when taken with Sulfasalazine
Sulindac (Compound) binds PTGS1 (Gene) and PTGS1 (Gene) is bound by Balsalazide (Compound) and Balsalazide (Compound) resembles Sulfasalazine (Compound)
Sulindac (Compound) binds PTGDR2 (Gene) and PTGDR2 (Gene) is bound by Indomethacin (Compound) and Indomethacin may cause a moderate interaction that could exacerbate diseases when taken with Sulfasalazine
Sulindac (Compound) binds CYP1A2 (Gene) and CYP1A2 (Gene) is bound by Phenobarbital (Compound) and Phenobarbital may cause a minor interaction that can limit clinical effects when taken with Sulfasalazine
Sulindac (Compound) binds PTGS1 (Gene) and PTGS1 (Gene) is associated with ulcerative colitis (Disease) and ulcerative colitis (Disease) is treated by Sulfasalazine (Compound)
Sulindac (Compound) binds AKR1B1 (Gene) and AKR1B1 (Gene) regulates ACAT1 (Gene) and ACAT1 (Gene) is bound by Sulfasalazine (Compound)
Sulindac (Compound) binds AKR1B1 (Gene) and AKR1B1 (Gene) regulates UBQLN2 (Gene) and UBQLN2 (Gene) is downregulated by Sulfasalazine (Compound)