Glycopyrrolate is a synthetic anticholinergic agent with a quaternary ammonium structure. Glycopyrrolate is a muscarinic competitive antagonist used as an antispasmodic, in some disorders of the gastrointestinal tract, and to reduce salivation with some anesthetics. Glycopyrrolate binds competitively to the muscarinic acetylcholine receptor. Like other anticholinergic (antimuscarinic) agents, it inhibits the action of acetylcholine on structures innervated by postganglionic cholinergic nerves and on smooth muscles that respond to acetylcholine but lack cholinergic innervation. These peripheral cholinergic receptors are present in the autonomic effector cells of smooth muscle, cardiac muscle, the sinoatrial node, the atrioventricular node, exocrine glands and, to a limited degree, in the autonomic ganglia. Thus, it diminishes the volume and free acidity of gastric secretions and controls excessive pharyngeal, tracheal, and bronchial secretions. Glycopyrrolate antagonizes muscarinic symptoms (e.g., bronchorrhea, bronchospasm, bradycardia, and intestinal hypermotility) induced by cholinergic drugs such as the anticholinesterases. The highly polar quaternary ammonium group of glycopyrrolate limits its passage across lipid membranes, such as the blood-brain barrier, in contrast to atropine sulfate and scopolamine hydrobromide, which are highly non-polar tertiary amines which penetrate lipid barriers easily. Glycopyrrolate is marketed under the brand names Robinul, Robinul Forte, Cuvposa. In October 2015, glycopyrrolate was approved by the FDA for use as a standalone treatment for Chronic obstructive pulmonary disease (COPD), as Seebri Neohaler.

Danusertib is a serine/threonine kinase inhibitor of multiple kinases, including aurora-A, B, and C. It also inhibits several cancer related tyrosine kinases as well as Abl, Trk-a, fibroblast growth receptor-1 and Ret. Danusertib is in phase II trials for the treatment of solid tumours, prostate cancer and chronic myeloid leukemia (CML). The most frequently reported side effects were neutropenia, nausea, anorexia, fatigue, and diarrhea.

Tozasertib, originally developed as VX-680 by Vertex (Cambridge, MA) and later renamed MK-0457 by Merck (Whitehouse Station, NY), was the first aurora kinase inhibitor to be tested in clinical trials. The drug, a pyrimidine derivative, has affinity for all aurora family members at nanomolar concentrations with inhibitory constant values (Ki(app)) of 0.6, 18, and 4.6 nM for aurora A, aurora B, and aurora C, respectively. Preclinical studies confirmed that tozasertib inhibited both aurora A and aurora B kinase activity, and activity has been reported against prostate, thyroid, ovarian, and oral squamous cancer cell lines. Upon treatment with tozasertib, cells accumulate with a 4N DNA content due to a failure of cytokinesis. This ultimately leads to apoptosis, preferentially in cells with a compromised p53 function. Tozasertib is an anticancer chemotherapeutic pan-aurora kinase (AurK) inhibitor that also inhibits FMS-like tyrosine kinase 3 (FLT3) and Abl. Tozasertib is currently in clinical trials as a potential treatment for acute lymphoblastic leukemia (ALL). In cellular models of cancer, tozasertib activates caspase-3 and PARP and decreases expression of HDAC, increasing apoptosis and inhibiting cell growth. In other cellular models, tozasertib inhibits cell proliferation and metastasis by blocking downstream ERK signaling and downregulating cdc25c and cyclin B. This compound also decreases tumor growth in an in vivo model of prostate cancer.

Alvameline is a partial agonist of the M1 mAChR that also displays M2/M3 antagonist effects. It readily crosses the blood-brain barrier. It has an effect profile that makes it of interest to test its ability to counteract bladder overactivity in humans. Behaviorally, alvameline has been shown to significantly improve Morris water maze (MWM) performance in both young and ageimpaired rats. It failed to improve cognition in patients with mild to moderate Alzheimer's disease.

Lysergide (LSD) is a semi-synthetic hallucinogen and is one of the most potent drugs known. Recreational use became popular between the 1960s to 1980s, but is now less common. LSD was first synthesized by Albert Hoffman while working for Sandoz Laboratories in Basel in 1938. Some years later, during a re-evaluation of the compound, he accidentally ingested a small amount and described the first ‘trip’. During the 1950s and 1960s, Sandoz evaluated the drug for therapeutic purposes and marketed it under the name Delysid®. It was used for research into the chemical origins of mental illness. Recreational use started in the 1960s and is associated with the ‘psychedelic period’. LSD possesses a complex pharmacological profile that includes direct activation of serotonin, dopamine and norepinephrine receptors. In addition, one of its chief sites of action is that of compound-specific (“allosteric”) alterations in secondary messengers associated with 5HT2A and 5HT2C receptor activation and changes in gene expression. The hallucinogenic effects of LSD are likely due to agonism at 5HT2A and 5HT2C receptors. LSD is also an agonist at the majority of known serotonin receptors, including 5HT1A, 5HT1B, 5HT1D, 5HT5A, 5HT6 and 5HT7 receptors. During the 1960s, LSD was investigated for a variety of psychiatric indications, including the following: as an aid in treatment of schizophrenia; as a means of creating a "model psychosis"; as a direct antidepressant; and as an adjunct to psychotherapy. LSD is listed in Schedule I of the United Nations 1971 Convention on Psychotropic Substances.

Dovitinib is an orally active small molecule that exhibits potent inhibitory activity against multiple receptor tyrosine kinases (RTK) involved in tumor growth and angiogenesis. Dovitinib strongly binds to fibroblast growth factor receptor 3 (FGFR3) and inhibits its phosphorylation, which may result in the inhibition of tumor cell proliferation and the induction of tumor cell death. In addition, this agent may inhibit other members of the RTK superfamily, including the vascular endothelial growth factor receptor; fibroblast growth factor receptor 1; platelet-derived growth factor receptor type 3; FMS-like tyrosine kinase 3; stem cell factor receptor (c-KIT); and colony-stimulating factor receptor 1; this may result in an additional reduction in cellular proliferation and angiogenesis, and the induction of tumor cell apoptosis. There are several ongoing Phase I/III clinical trials for dovitinib.

AMG-487 is a potent and selective orally bioavailable chemokine (C-X-C motif) receptor 3 (CXCR3) antagonist that displays dose- and time-dependent pharmacokinetics in human subjects after multiple oral dosing. AMG-487 is an 8-azaquinazolinone, it can prevent the chemokines I-IP-10 and I-ITAC from binding to CXCR3. The preclinical properties of AMG487 has been extensively studied. The compound displays a greater than 1000-fold selectivity for CXCR3 versus a panel of other receptors, including 11 chemokine receptors. The safety profile of AMG487, as assessed by various genotoxicity and cardiotoxicity assays, revealed no major concerns. The ability of AMG487 to inhibit inflammatory cell migration in vivo was confirmed in a mouse model of bleomycin-induced cellular recruitment, where AMG487 significantly reduced infiltration of macrophages and lymphocytes into the lungs in CXCR3-KO mice. In a mouse model for idiopathic pneumonia syndrome (IPS), AMG487 reduced recruitment of donor T cells to the lung after allogeneic stem cell transplantation, leading to improved survival rates. Likewise, reductions in inflammation, pannus formation, and cartilage damage were observed upon administering AMG487. The preclinical studies convincingly paved the way for clinical studies on two inflammation-related diseases: psoriasis and rheumatoid arthritis. In 2003, results of a Phase I trial on AMG487 were disclosed. The compound was assessed for safety and pharmacokinetics in 30 healthy males in a randomised, double blind, placebo-controlled dose-escalation study. Generally, the compound was well tolerated and adverse events were mild to moderate. Disappointingly, no significant differences in the endpoints (psoriasis severity index or physician global assessment scores) were seen between patient groups. AMG-487 progressed to Phase II clinical trials but has been withdrawn because of lack of efficacy.

Itopride is a dopamine D2 receptor antagonist and inhibitor of acetylcholinesterase. It is indicated in the for the treatment of gastrointestinal symptoms caused by reduced gastrointestinal motility, such as functional non-ulcer dyspepsia (chronic gastritis), gastric fullness, rapid satiation, pain or discomfort in the upper abdomen, anorexia, heartburn, nausea, and vomiting. The drug is not approved in the USA or UK but is available in Japan and Western European countries.

Benzydamine (benzydamine hydrochloride, PHARIXIA®) is a benzyl-indazole having analgesic, antipyretic, and anti-inflammatory effects. It is indicated for the relief of pain in acute sore throat and for the symptomatic relief of oro-pharyngeal mucositis caused by radiation therapy.

Fenthion (trade names include Baytex™, Baycid™, and Tiguvon™, used on livestock) was first registered domestically in 1965 by the Mobay Corp., a U.S. subsidiary of Bayer AG of West Germany. Fenthion is a contact and stomach insecticide used against many sucking, biting pests, especially fruit flies, stem borers, mosquitoes, and Eurygaster cereal bugs. In mosquitoes, it is toxic to both the adult and immature forms (larvae). Once used extensively in the U.S. for controlling intestinal worms, fenthion no longer has FDA approval due to an excess number of poisoning deaths. Like most other organophosphates, its mode of action is via cholinesterase inhibition. It was used mostly for the control of grubs and lice in beef and nonlactating cattle.