2-[18F]Fludarabine is a Positron Emission Tomography (PET) tracer for imaging lymphoma.

AZD9164 was invented by AstraZeneca as a muscarinic M(3) receptor antagonist for evaluation of the potential as a treatment for chronic obstructive pulmonary disease. However, in 2010 studies were discontinued.

Volixibat (SHP626; formerly LUM002) is a potent inhibitor of the apical sodium-dependent bile acid transporter (ASBT) that was developed for the treatment of nonalcoholic steatohepatitis. Volixibat participated in phase II clinical trial to investigate its safety, effectiveness in adults with nonalcoholic steatohepatitis. However, this study was discontinued, without any further explanation for the possible causes. In addition, volixibat was studied in a clinical trial in healthy adults and in patients with type 2 diabetes mellitus, where was shown that the drug was generally well tolerated.

Diclobutrazol is the active ingredient of a broad-spectrum systemic fungicide for use on cereals. Diclobutrazol sprays appear promising for the control of coffee rust, apple mildew and scab, grape powdery mildew and various other crop diseases. Diclobutrazol has a systemic action and is translocated mainly acropetally. It eradicative action, increased by vapour effect, is very strong. Diclobutrazol is of low toxicity to mammals and other animals. It is also of low toxicity to birds, fish and invertebrates. Diclobutrazol inhibited spore germination and mycelia growth of a wide range of fungi. Stereoselective inhibition of human CYP3A4 and Candida albicans CYP51 was observed with enantiomers of the azole antifungal compound diclobutrazol. The RR(+) configuration at its asymmetric carbon center was most active.

Phosphopantothenic acid is an amidoalkyl phosphate that is the 4-phosphate derivative of (R)-pantothenic acid. Phosphopantothenic acid is not permeable to cell membranes due to its anionic character, consistent with the observation that systemic administration of Phosphopantothenic acid does not restore CoA levels in cellular and mouse models

(±)-quinuclidinyl benzilate (3-quinuclidinyl benzilate), is a specific muscarinic cholinergic receptor antagonist. It binds potently but reversibly to the muscarinic cholinergic receptors of mammalian brain and peripheral tissues. 3-quinuclidinyl benzilate was invented by Hoffmann-La Roche Inc in 1951, while investigating antispasmodic agents resembling tropine for the treatment of gastrointestinal conditions. In the 1960s 3-quinuclidinyl benzilate, was developed and weaponized as a new chemical agent for battlefield use as a psychochemical. Assigned the NATO code BZ it is classified as a hallucinogenic chemical warfare agent that affects both the peripheral and central nervous systems (CNS). It is one of the most potent anticholinergic psychomimetics known, with only small doses necessary to produce incapacitation. The primary route of absorption is through the respiratory system but absorption also can occur through the skin or gastrointestinal tract. BZ is odorless and is usually disseminated as an aerosol. Data regarding the health effects of BZ in humans following inhalation exposure are limited to military application studies. Pharmacologic activity of 3-quinuclidinyl benzilate is similar to other anticholinergic drugs (eg, atropine) but with a much longer duration of action. It was shown that I[3H]-3-quinuclidinyl benzilate accumulated in various brain regions after intravenous injection. The specific binding of [3-3H]3-quinuclidinyl-benzilate and [125I]3-quinuclidinyl-(3-iodo-4-hydroxy-benzilate) to rat brain subcellular fractions is parallel in myelin, synaptic plasma membrane and mitochondrial fractions with a 3-4-fold enrichment observed in synaptic plasma membrane over crude mitochondrial fractions. These findings suggested the use of 3-quinuclidinyl benzilate as a binding probe useful in assaying low levels of muscarinic receptor in tissue culture and other biological sources including labeling the receptor in vivo for autoradiographic studies. M2 muscarinic acetylcholine receptor (M2 receptor), essential for the physiologic control of cardiovascular function through activation of G protein-coupled inwardly-rectifying potassium channels, was shown to bind 3-quinuclidinyl benzilate with high affinity in vitro.