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.

(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.

(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.

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.

(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.

(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.