Ditekiren is a relatively large renin inhibitor incorporating the hydroxyethylene isostere as well as both the P4 proline and P2’ isoleucine of angiotensinogen. Methylation of the P2-site histidine backbone nitrogen stabilizes the P2-P3 peptide bond towards degradation by chymotrypsin. Even though oral bioavailability was low, serum ditekiren levels were equivalent to 4–8 times the in vitro IC50 for renin inhibition for this peptide throughout the 2.5 h after oral administration that blood levels were monitored. In Na-depleted cynomolgus monkeys, oral dose elicited a hypotensive response that had not returned to baseline by 5 h. Ditekiren had been in phase II clinical trials for the treatment of heart failure and hypertension. However, these studies were discontinued.

Xenbucin is an antihyperlipidemic agent. Information about the current use of this agent is not available.

FENOCINOL, a diarylmethane derivative, is a choleretic agent.

Axitirome (also known as CGS 26214), a thyroid hormone receptor β selective agonist and an LDL receptor function stimulant, has a cholesterol-lowering activity. This drug was in phase I clinical trials for the treatment of hyperlipidemia, but studies were discontinued because of the unexpected side effects.

Naxifylline [CVT 124, BG 9719], a small molecule diuretic, is one of a new class of potent and highly selective adenosine A1 receptor antagonists discovered at University of Florida. Naxifylline is an A1 adenosine receptor antagonist used for the treatment of edema associated with congestive heart failure. Naxifylline appears to be one of the more potent and clearly the most A1-selective antagonist reported to date, with K1 values of 0.67 and 0.45 nM, respectively, at the rat and cloned human A1-receptors and with 1800-fold (rat) and 2400-fold (human) subtype selectivity. Naxifylline protects against the decline in renal function observed with diuretic therapy by promoting urine output.

Famprofazone, a nonsteroidal anti-inflammatory agent, is found in a multi-ingredient medication (Gewodin) used for pain relief. It is available over-the-counter in Taiwan. Famprofazone transforms to methamphetamine (MA) and amphetamine (AM) following administration, which is responsible for the side effects of the drug. For example, famprofazone user might be interpreted as an illicit MA abuser in Taiwan because the user's urine tested positive for MA.

Losigamone possesses an unique anticonvulsant activity profile and has an excellent tolerability. Losigamone causes dose-dependent inhibition of the tonic hind leg extension produced by electric shock, pentylenetetrazole, bicuculline, nicotine and 4-aminopyridine. Losigamone also inhibits clonic seizures induced by pentylenetetrazole, bicuculline and picrotoxin, whereas it has no effect on the hind leg extension caused by strychnine and picrotoxin or the clonic seizures induced by NMDA. Losigamone had been in phase III clinical trial for the treatment of partial epilepsies. However, this development was discontinued.

Dexbudesonide (22R- Budesonide) is an epimer R of Budesonide, last is used as a mixture of 22R and 22S epimers for the topical treatment of asthma, rhinitis, and inflammatory bowel disease

Cipemastat (Ro 32-3555, tentative trade name Trocade) is a dipeptide, potent, competitive inhibitor of matrix metalloproteinases (MMP) 1, 8 and 13, which was under development by Roche for the potential treatment of rheumatoid arthritis. Cipemastat is a selective inhibitor of metalloproteinases 1, 8 and 13 over the related human matrix metalloproteinases stromelysin 1, and gelatinases A and B. Cipemastat mediated MMP inhibition leads to block the final common event in the destructive cascade resulting in the breakdown of cartilage and bone. Trocade has also been shown to inhibit cartilage destruction in vivo and to prevent structural joint damage in animal models of rheumatoid and osteoarthritis. Cipemastat was in phase II clinical trials for the treatment of rheumatoid arthritis. However, Roche discontinued the development of cipemastat because of an unfavorable risk-benefit profile.

Brolamfetamine (also known as DOB, bromo-DMA, and 4-bromo-2,5-dimethoxyphenylisopropylamine) is one of a vast number of compounds used recreationally to achieve hallucinogenic effects. Brolamfetamine is one of the most potent hallucinogens, with its hallucinogenic potency directly linked to its abuse potential. Brolamfetamine acts as a partial agonist of 5HT2A, 5HT2B, 5HT2C, and TAAR1 receptors, but it’s psychedelic effects are mainly mediated by its agonistic properties at the 5-HT2A receptor. Animal studies have shown physiologic effects including hypertension, tachycardia, hyperpyrexia, pupillary dilatation, and peripheral vasoconstriction. In general, Brolamfetamine having a similar effect to LSD, with slower onset (up to 3–4 h to peak intoxication) and longer duration of effect (up to 36 h). Brolamfetamine is not commonly available, through periods of higher circulation were reported in Australia in 1983, Ireland in 2003, and in Italy in 2015. Brolamphetamine, as well as many other synthetic hallucinogens, are increasingly being sold as LSD. Internationally Brolamfetamine is a Schedule I drug under the Convention on Psychotropic Substances. Due to its selectivity, Brolamfetamine is often used in scientific research when studying the 5-HT2 receptor subfamily.