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Restrict the search for
sulindac
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There is one exact (name or code) match for sulindac
Status:
US Approved Rx
(1991)
Source:
ANDA072050
(1991)
Source URL:
First approved in 1978
Source:
CLINORIL by MERCK
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Sulindac is a nonsteroidal anti-inflammatory agent (NSAIA) of the arylalkanoic acid class that is marketed in the U.S. by Merck as Clinoril. Like other NSAIAs, 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. The sulfide metabolite then undergoes enterohepatic circulation; it is excreted in the bile and then reabsorbed from the intestine. This is thought to help maintain constant blood levels with reduced gastrointestinal side effects. Some studies have shown sulindac to be relatively less irritating to the stomach than other NSAIA's except for drugs of the cyclooxygenase-2 (COX-2) inhibitor class. The exact mechanism of its NSAIA properties is unknown, but it is thought to act on enzymes COX-1 and COX-2, inhibiting prostaglandin synthesis.
Status:
US Approved Rx
(1991)
Source:
ANDA072050
(1991)
Source URL:
First approved in 1978
Source:
CLINORIL by MERCK
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Sulindac is a nonsteroidal anti-inflammatory agent (NSAIA) of the arylalkanoic acid class that is marketed in the U.S. by Merck as Clinoril. Like other NSAIAs, 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. The sulfide metabolite then undergoes enterohepatic circulation; it is excreted in the bile and then reabsorbed from the intestine. This is thought to help maintain constant blood levels with reduced gastrointestinal side effects. Some studies have shown sulindac to be relatively less irritating to the stomach than other NSAIA's except for drugs of the cyclooxygenase-2 (COX-2) inhibitor class. The exact mechanism of its NSAIA properties is unknown, but it is thought to act on enzymes COX-1 and COX-2, inhibiting prostaglandin synthesis.
Status:
US Approved Rx
(2023)
Source:
NDA215500
(2023)
Source URL:
First approved in 1990
Source:
ORNIDYL by SANOFI AVENTIS US
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Conditions:
Eflornithine is a prescription drug indicated in the treatment of facial hirsutism (excessive hair growth). Eflornithine hydrochloride cream for topical application is intended for use in women suffering from facial hirsutism and is sold by Allergan, Inc. under the brand name Vaniqa. Besides being a non-mechanical and non-cosmetic treatment, eflornithine is the only non-hormonal and non-systemic prescription option available for women who suffer from facial hirsutism. Eflornithine for injection against sleeping sickness was manufactured by Sanofi Aventis and sold under the brand name Ornidyl in the USA. It is now discontinued. Eflornithine is on the World Health Organization's List of Essential Medicines. Eflornithine prevents hair growth by inhibiting the anagen phase of hair production. This occurs by eflornithine irreversibly binding (also called suicide inhibition) to ornithine decarboxylase (ODC) and physically preventing the natural substrate ornithine from accessing the active site.
Status:
Investigational
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Exisulind (tentative trade name Aptosyn) is an antineoplastic agent, which was originally developed by Cell Pathways. This drug is an inhibitor of phosphodiesterase (PDE) isozymes: PDE5 and PDE4. Inhibition of PDE5 appears to be pharmacologically relevant, which leads to increase cGMP and activate protein kinase G at doses that induce apoptosis, whereas cyclic AMP levels were not changed. Exisulind has been in phase III clinical trials for the treatment of Non-Small Cell Lung Cancer and for the treatment of polyps in patients who have familial adenomatous polyposis (Colorectal Cancer and Small Intestine Cancer). In addition, this drug was in phase II/III for the treatment of Prostate Cancer, however, there studies have been discontinued.
Status:
Other
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Sulindac sulfide, an active metabolite of the nonsteroidal anti-inflammatory drug (NSAID) sulindac, directly binds to the Ras gene product p21ras in a non-covalent manner. Sulindac sulfide strongly inhibits Ras-induced malignant transformation and Ras/Raf dependent transactivation, due to its action at the most critical site in Ras signaling. Sulindac sulfide was proposed as a lead compound in the search for novel anti-cancer drugs, which directly inhibit Ras-mediated cell proliferation and malignant transformation. Experiments on rodents have revealed that sulindac sulfide effectively inhibited tumor growth in colorectal cancer cell xenografts mice. In addition, was shown, that sulindac sulfide inhibited ABCC1-mediated transport of appropriate endogenous and xenobiotic substrates. The drug was selectivity for ABCC1 as compared with ABCB1 and ABCG2. These properties allow designing novel ABCC1 inhibitors by chemically modifying sulindac sulfide to improve potency and selectivity to inhibit ABCC1-mediated efflux for preventing drug resistance and tumor recurrence or secondary tumor formation following chemotherapy.
Status:
Possibly Marketed Outside US
Source:
SULINDAC by Fillet, M.|Hubert, P.|Crommen, J.
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
(R)-Sulindac is the (R)-enantiomer of nonsteroidal anti-inflammatory drug (NSAID) Sulindac, that is marketed in the U.S. by Merck as Clinoril. Sulindac is a prodrug, derived from sulfinylindene, that is converted in vivo to an active sulfide compound by liver methionine sulfoxide reductases (Msr). The (Msr) family of enzymes includes two major classes, MsrA and MsrB, that specifically reduce the S- and R-epimers of Sulindac. Reduction of (R)-Sulindac to Sulindac Sulfide catalyzed by methionine sulfoxide reductase (Msr)-B. The oxidation of both epimers to sulindac sulfone is catalyzed primarily by the microsomal cytochrome P450 (P450) system. (S)-Sulindac increases the activity of the P450 system better than (R)-sulindac, but both epimers increase primarily the enzymes that oxidize (R)-sulindac. Both epimers can protect normal lung cells against oxidative damage and enhance the killing of lung cancer cells exposed to oxidative stress.
Status:
Possibly Marketed Outside US
Class (Stereo):
CHEMICAL (ABSOLUTE)
(S)-Sulindac is the (S)-enantiomer of nonsteroidal anti-inflammatory drug (NSAID) Sulindac, that is marketed in the U.S. by Merck as Clinoril. Sulindac is a prodrug, derived from sulfinyl-indene, that is converted in vivo to an active sulfide compound by liver methionine sulfoxide reductases (Msr). The (Msr) family of enzymes includes two major classes, MsrA and MsrB, that specifically reduce the S- and R-epimers of Sulindac. Reduction of (S)-Sulindac to Sulindac Sulfide catalyzed by methionine sulfoxide reductase (Msr)-A. The oxidation of both epimers to sulindac sulfone is catalyzed primarily by the microsomal cytochrome P450 (P450) system. (S)-Sulindac increases the activity of the P450 system better than (R)-sulindac, but both epimers increase primarily the enzymes that oxidize (R)-sulindac. Both epimers can protect normal lung cells against oxidative damage and enhance the killing of lung cancer cells exposed to oxidative stress.
Status:
Possibly Marketed Outside US
Source:
Octaplasma by Octapharma Pharmazeutika Produktionsges M B H [Canada]
Source URL:
First approved in 2013
Source:
BLA125416
Source URL:
Class:
MIXTURE
