Primisulfuron-methyl is a urea herbicide that is used on crop and non- crop areas for the control of grass weeds and many kinds of broad-leaved weeds. Primisulfuron-methyl is a selective postemergence systemic herbicide that is rapidly absorbed by plants and transported throughout the plant roots and foliage. The herbicide works by blocking cell growth in the active growing regions of the plant. Primisulfuron-methyl is practically non-toxic by ingestion, with a reported oral LD50 of greater than 5050 mg/kg in rats. Primisulfuron-methyl is practically nontoxic to wildfowl. Both bobwhite quail and mallard ducks show a high tolerance for the compound. Primisulfuron-methyl is of low to moderate persistence in the soil environment, with a field half-life of from 4 to 60 days. A representative value is estimated to be about 30 days.

Chlorpyrifos-methyl is a broad-spectrum organophosphorous insecticide and potential toxic pollutant widely used in agriculture and effective against a wide range of insect pests in commercial importance crops. Chlorpyrifos-methyl have endocrine disruption activity, especially anti-androgenic effects and Chlorpyrifos-methyl administration leads to hepatotoxicity and neurotoxicity in mammals. The fish exposed to chlorpyrifos-methyl exhibited behavioral changes in the form of neurotoxin toxicity: less general activity than control group, loss of equilibrium, erratic swimming and staying motionless at a certain location

2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is a mutagenic and carcinogenic heterocyclic amine formed during ordinary cooking, and is subsequently metabolically activated by cytochrome P4501A2 (CYP1A2) and N-acetyltransferase 2 (NAT2). PhIP has been used in trials studying the basic science of Pancreas Cancer.

Bardoxolone methyl, the C-28 methyl ester of 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid (CDDO) known as CDDO-Me or RTA 402, is one of the derivatives of synthetic triterpenoids. Bardoxolone methyl directly blocks IKKbeta activity and thereby the NF-kappaB pathway by interacting with Cys-179 in the IKKbeta activation loop. Binding of bardoxolone methyl to Kelch-like erythroid cell-derived protein with CNC homology-associated protein 1 (Keap1) disrupts its critical cysteine residues, leading to the release of the nuclear factor erythroid 2-related factor 2 (Nrf2), which hinders its ubiquitination and finally leads to its stabilization and nuclear translocation. In the nucleus, Nrf2 activates the transcription of phase 2 response genes, leading to a coordinated antioxidant and anti-inflammatory response. In addition, it acts as an antagonist of the peroxisome proliferator-activated receptor gamma. Through Keap1/Nrf2 and nuclear factor-κB pathways, this agent can modulate the activities of a number of important proteins that regulate inflammation, redox balance, cell proliferation and programmed cell death. This agent is generally well tolerated, but it may increase adverse cardiovascular events. Presently, it is being further tested for the treatment of patients with chronic kidney disease, cancer, and pulmonary arterial hypertension.