9cUAB30 is a synthetic analog of 9-cis-RA with little or no RAR-binding activity relative to 9-cis-RA and other RA. 9cUAB30, is a selective rexinoid for the retinoid X nuclear receptors (RXR). Retinoid 9cUAB30 binds to and activates retinoid X receptor (RXR) homodimers and/or and retinoic acid receptor (RAR)/RXR heterodimers, which may result in the dissociation of corepressor protein and the recruitment of coactivator protein, followed by transcription of downstream target genes into mRNAs and protein translation. Gene transcription regulated by these transcription factors may result in inhibition of cell proliferation, induction of cell differentiation, and apoptosis of both normal cells and tumor cells. 9cUAB30 displays substantial chemopreventive capacity with little toxicity and is being translated to the clinic as a novel cancer prevention agent. 9cUAB30 has been assessed in vitro with human cell cultures. Human hepatocytes demonstrated no signs of cytotoxicity with treatment of 9cUAB30 up to 50 umol/L, although when human breast cancer cells were treated with 9cUAB30, they showed a significant inhibition of cell proliferation and apoptotic levels 2.5to 3.5 times the levels of untreated cells. 9cUAB30 inhibits telomerase and induces apoptosis in HL60 cells.

Deferitrin is a desferrithiocin-derived hexadentate iron chelator, developed by Genzyme Corp. for the treatment of severe iron overload in people who require repeated erythrocyte transfusion for the management of chronic anemia such as beta-thalassemia major. Development of the drug was halted after phase 1/2 clinical trial due to nephrotoxicity.

D-aspartic acid is an essential amino acid and a key ingredient in various testosterone boosting anti-estrogen supplements. D-aspartic acid is not used to build proteins; instead, it plays a role in making and releasing hormones in the body. It is an endogenous NMDA receptor agonist with similar activity to the L-isomer. D-aspartic acid also enhances the release of luteinizing hormone (LH) and testosterone. This action is mediated in the pituitary by cGMP and in the testis by cAMP, which acts as the second messengers in the signal transduction in the pituitary and testes respectively. The pituitary and testis possess a D-Aspartate racemase, which provides the necessary production of this isomer.

Chlorogenic acid is the ester of caffeic acid and (-)-quinic acid. Chlorogenic acid is a naturally occurring plant metabolite and can be found with the related compounds cryptochlorgenic acid and neochlorogenic acid in the leaves of Hibiscus sabdariffa, coffee, potato, eggplant, peaches, and prunes. Chlorogenic acid has been investigated as a dietary supplement to improve glucose intolerant hypoglycemia and non-alcoholic fatty liver disease. It has also been identified as a potential anticancer agent by reducing the expression of HIF-1a and Sphingosine Kinase-1. Chlorogenic acid was also identified as a neuraminidase blocker effective against influenza A virus (H1N1 and H3N2).

Methylmalonic acid (MMA) is a C-methylated derivative of malonate. Elevated levels of methylmalonic acid result from inherited defects of enzymes involved in MMA metabolism or inherited or acquired deficiencies of vitamin B12 or its downstream metabolites. MMA is also a specific diagnostic marker for the group of disorders collectively called methylmalonic acidemia.

Tridecanoic acid is a 13-carbon saturated fatty acid found in dairy products and also as a product of anaerobic biodegradation of n-hexadecane. It has been identified as a substrate of phospholipase A2. Saturated fatty acids with carbon chain lengths of C12 to C14 activated the alpha-, beta-, gamma-, and epsilon-subspecies of the protein kinase C, and this activation was synergistic with that by diacylglycerol. Tridecanoic acid(C13) was most effective among the saturated fatty acids examined.

Avoralstat, a small molecule inhibitor of plasma kallikrein, participated in clinical trials phase III to prevent hereditary angioedema, but these studied were discontinued due to insufficient efficacy study. Recently published article has described that avoralstat could improve the quality of life in C1‐INH‐HAE patients. Hereditary angioedema (HAE) with C1 inhibitor deficiency (C1‐INH‐HAE) is an autosomal dominant disorder characterized by recurrent episodes of swelling of the skin, pharynx, gastrointestinal tract, genitals, and is due primarily to mutations in the SERPING1 gene that results in insufficient production of the natural plasma kallikrein inhibitor, C1 inhibitor (C1‐INH).

Adarotene (ST1926) is a new pro-apoptotic and cytodifferentiating antitumour drug, belongs to the so-called class of atypical retinoids. Adarotene is active on its own or in combination with other chemotherapeutics for the treatment of a vast number of experimental tumors. It was found in preclinical investigations the potential therapeutic use it in chronic myeloid leukemia (CML), against Rhabdomyosarcoma and for treatment of Adult T-cell leukemia/lymphoma (ATL). ST1926 induced an early DNA damage response, which led to increase in apoptosis, in addition to S-phase cell cycle arrest and a reduction in protein levels of the cell cycle kinase CDK1. The presence of the phenolic hydroxyl group on adarotene structure allows a rapid O-glucuronidation as a major mechanism of elimination of the drug, favoring a fast excretion of its glucuronide metabolite in the urines.

Etarotene (Ro 15-1570) is an arotinoid sulfone. Etarotene inhibits RNase P, a ribonucleoprotein that endonucleolytically cleaves all tRNA precursors to produce the mature 5' end, thereby affecting tRNA biogenesis. Etarotene has antikeratinizing potential. It was undergoing phase III clinical trials with Roche in the US for the treatment of psoriasis and other skin.