Clozapine N-oxide is a phase 1 metabolite of antipsychotic drug clozapine, produced by oxidation of clozapine by CYP3A4. Clozapine N-oxide is inert with respect to a wide range of GPCRs. It was used a tool compound in the DREADD (designer receptors exclusively activated by designer drugs) system in which a mutated muscarinic G protein-coupled receptor is activated by an otherwise inert compound, however interpretation of experiments is confounded by the ability of clozapine-N-oxide to convert to clozapine upon administration. Clozapine N-oxide exhibits neuroprotective action by inhibiting of microglial NADPH oxidase.

Genz-123346 is a potent and selective glucosylceramide synthase (GCS) inhibitor that blocks the conversion of ceramide to GL1. It has been studied as a potential treatment of diabetes mellitus, polycystic kidney disease and fatty liver disease. Genz-123346 improved glucose tolerance and increased insulin sensitivity in two animal models of type 2 diabetes. In Zucker diabetic fatty rats, treatment with Genz-123346 significantly lowered blood glucose levels and partially prevented the normal deterioration of pancreatic β-cell function over time and preserved the ability of the islets to secrete insulin. In the high-fat–fed diet-induced obese mice, Genz-123346 essentially normalized A1C levels to that of the lean animals. Inhibiting GSL synthesis ameliorates the liver pathology associated with obesity and diabetes in mice model. Blockade of kidney glucosylceramide GlcCer accumulation with the GCS inhibitor Genz-123346 effectively inhibits cystogenesis in mouse models orthologous to human autosomal dominant polycystic kidney disease (PKD) (Pkd1 conditional knockout mice) and nephronophthisis (jck and pcy mice). Molecular analysis in vitro and in vivo indicated that inhibition of GCS by Genz-123346 inhibited the AKT-mTOR signaling pathway. It induced autophagy via the AKT-mTOR signaling pathway in HEK293T cells, increased autophagy flux and reduced mutant α-syn levels in mouse primary neurons potentially via indendent mechanisms. Exposure of cells to Genz-123346 and to other GCS inhibitors at non-toxic concentrations can enhance the killing of tumor cells by cytotoxic anti-cancer agents. This chemosensitizing activity was unrelated to lowering intracellular glycosphingolipid levels. Genz-123346 is a substrate for multi-drug resistance efflux pumps such as P-gp (ABCB1, gP-170). In cell lines selected to over-express P-gp or which endogenously express P-gp, chemosensitization by Genz-123346 was primarily due to the effects on P-gp function. Genz-123346 has little effect on 1-O-acylceramide synthase activity at concentrations that effectively inhibit GL1 synthase activity and therefore do not significantly elevate cell ceramide levels in vitro. Unlike N-butyldeoxynojirimycin (NB-DNJ), another inhibitor of GCS Genz-123346 does not inhibit α-glucosidase or glucocerebrosidase.

3,4-Dicaffeoylquinic acid is a component of Brazilian green propolis water extract, green coffee beans and other plants. It was reported to have antivirus activity against Influenza A Virus. The compound was also shown to inhibit AngII-induced rVSMC proliferation and migration, probably through downregulating the Akt, JNK and part of the ERK1/2 pathways, in which the anti-oxidant property plays an important role. 3,4-Dicaffeoylquinic acid possesses a high binding affinity to plasma proteins, making it less preferable as a drug candidate as this characteristic would affect diffusion or transport across cell membranes, limiting pharmacological actions. 3,4-Dicaffeoylquinic acid is also a selective inhibitor of human immunodeficiency virus type 1 integrase.

SB-431542 was identified as a TGF-beta receptor type-1 inhibitor (IC50 = 94 nM) by scientists at GlaxoSmithKline. It has subsequently been studied in animal and cell models as a potential cancer treatment, although these efforts have been discontinued. Of note, SB-431542 was also used in a wound healing study where it was found to abolish the improved healing normally enhanced by treatment with Povidone-iodine.

N-Desethyl Sunitinib is a major and pharmacologically active metabolite of sunitinib, which is potent, ATP-competitive VEGFR, PDGFRβ, and KIT inhibitor.

4-hydroxy-2-nonenal (4-HNE or HNE), a very reactive aldehyde derived from lipid peroxidation, is the product and mediator of oxidative stress. It can modulate a number of signaling processes mainly through forming covalent adducts with nucleophilic functional groups in proteins, nucleic acids, and membrane lipids. HNE is mutagenic and genotoxic because it reacts with all four DNA bases but with different efficiency: G >C > A >T. In addition, in the experiments with dogs was shown the pathophysiologic role of HNE in osteoarthritis.

(7AR)-7A-epi-Perindopril is an epimer (S, SR, SS) of the drug perindopril which is commonly used to treat high blood pressure, hypertension, heart failure, or stable coronary artery disease. This epimer possesses equal activity with the perindopril.

PF-998425 is a selective non-steroidal androgen receptor antagonist. It is rapidly metabolized systemically, and demonstrated efficacy for treatment of androgenic alopecia in preclinical model.

Cupric selenide (Cu2S) is a semiconductor, which is able to form nanocrystals. The nanocrystals were shown to be an effective photothermal material for the photothermal therapy application in cancer. In vitro photothermal heating of Cu2-xSe nanocrystals in the presence of human colorectal cancer cell (HCT-116) led to cell destruction after 5 min of laser irradiation at 33 W/cm2

Sabutoclax, an apogossypol derivative, also known as BI-97C1, functions as an inhibitor of all anti-apoptotic Bcl-2 proteins, including Bcl-XL, Bcl-2, Mcl-1, and Bfl-1. Sabutoclax induces cancer-specific cell death in a Mcl-1-dependent manner through both apoptosis and toxic mitophagy. Sabutoclax and COX-2 inhibitor, celecoxib, synergistically inhibit the growth of oral squamous cell carcinomas (OSCC) in vitro and significantly reduce OSCC tumor growth in vivo. These results identify Mcl-1 as a therapeutic prospective target in OSCC. Moreover, as shown, a combination regimen of tropism-modified adenovirus delivered mda-7/IL-24 (Ad.5/3-mda-7) and sabutoclax enhance cytotoxicity in human prostate cancer (PC) cells, including those resistant to mda-7/IL-24 or BI-97C1 alone, thus potentially augmenting the therapeutic benefit of this combinatorial approach toward PC.