Dimesna is a prodrug of mesna (dimer of mesna). Dimesna is reduced to mesna in the kidneys. Dimesna does not prevent cellular damage by metabolites of ifosfamide and cyclophosphamide in the renal tubular cell line LLC-PK1. Dimesna is a mucolytic agent used to alleviate toxic side effects of antitumor drugs. The organic acid transporter OAT4 on the luminal side of the proximal renal tubule facilitates the reabsorption of dimesna, and therefore its reduction to mesna, whereas the multidrug and toxin extrusion protein MATE1, the multidrug resistance protein MRP2, and P glycoprotein facilitate the efflux of mesna and/or dimesna back into the lumen; dimesna may also be excreted unchanged by MRP4. It has therefore been suggested that polymorphism of these renal transport proteins or transporter-mediated drug-drug interactions may reduce the efficacy of mesna and dimesna.

Monophosphothiamine is thiamine derivative used for the treatment of neuritis, polyneuritis, asthenic conditions (weakness), as an additional remedy for chronic blood circulation insufficiency, chronic gastritis accompanied by motor and secretory disorders functions of the stomach. Monophosphothiamine underwent metabolic phosphorylation to active metabolite thiamine pyrophosphate, that acts as a coenzyme in the different metabolic process.

Sodium sulfanilate is a salt of sulphanilic acid and has been used to monitor the degree of renal dysfunction in dogs.

Vaccenic acid (VA) (t11 octadecenoic acid) is a positional and geometric isomer of oleic acid (c9-octadecenoic acid), and is the predominant trans monoene in ruminant fats (50%–80% of total trans content). Dietary VA can be desaturated to cis-9,trans-11 conjugated linoleic acid (c9,t11-CLA) in ruminants, rodents, and humans. Hydrogenated plant oils are another source of VA in the diet, and it has been recently estimated that this source may contribute to about 13%–17% of total VA intake. In contrast to suggestions from the epidemiological studies, the majority of studies using cancer cell lines (Awad et al. 1995; Miller et al. 2003) or rodent tumors (Banni et al. 2001; Corl et al. 2003; Ip et al. 1999; Sauer et al. 2004) have demonstrated that VA reduces cell growth and (or) tumor metabolism. Animal and in vitro studies suggest that the anti-cancer properties of VA are due, in part, to the in vivo conversion of VA to c9,t11-CLA. However, several additional mechanisms for the anti-cancer effects of VA have been proposed, including changes in phosphatidylinositol hydrolysis, reduced proliferation, increased apoptosis, and inhibition of fatty acid uptake. In conclusion, although the epidemiological evidence of VA intake and cancer risk suggests a positive relationship, this is not supported by the few animal studies that have been performed. The majority of the studies suggest that any health benefit of VA may be conferred by in vivo mammalian conversion of VA to c9,t11-CLA. VA acts as a partial agonist to both peroxisome proliferator-activated receptors (PPAR)-α and PPAR-γ in vitro, with similar affinity compared to commonly known PPAR agonists. Hypolipidemic and antihypertrophic bioactivity of VA is potentially mediated via PPAR-/-dependent pathways.