Ixazomib (trade name Ninlaro) is a drug for the treatment of multiple myeloma in adults after at least one prior therapy, in combination with lenalidomide and dexamethasone. It is taken by mouth in form of capsules. Common side effects include diarrhea, constipation and low platelet count. Like the older bortezomib (which can only be given by injection), it acts as a proteasome inhibitor, has orphan drug status in the US and Europe. At therapeutic concentrations, ixazomib selectively and reversibly inhibits the protein proteasome subunit beta type-5 (PSMB5) with a dissociation half-life of 18 minutes. This mechanism is the same as of bortezomib, which has a much longer dissociation half-life of 110 minutes; the related drug carfilzomib, by contrast, blocks PSMB5 irreversibly. Proteasome subunits beta type-1 and type-2 are only inhibited at high concentrations reached in cell culture models. PSMB5 is part of the 20S proteasome complex and has enzymatic activity similar to chymotrypsin. It induces apoptosis, a type of programmed cell death, in various cancer cell lines. A synergistic effect of ixazomib and lenalidomide has been found in a large number of myeloma cell lines. The medication is taken orally as a prodrug, ixazomib citrate, which is a boronic ester; this ester rapidly hydrolyzes under physiological conditions to its biologically active form, ixazomib, a boronic acid. Absolute bioavailability is 58%, and highest blood plasma concentrations of ixazomib are reached after one hour. Plasma protein binding is 99%.

Triethyl citrate is a triester of ethyl alcohol and citric acid. It is a colorless, odorless liquid used as a food additive (E number E1505) to stabilize foams, especially as whipping aid for egg white. Triethyl citrate is a plasticizer, that plays an important role as a dispersing aid in the processing of polylactic acid/chitin nanocrystal (PLA/ChNC) nanocomposites.

Zuclomiphene Citrate is the cis isomer of clomiphene which exhibits weak estrogen agonist activity evaluated for antineoplastic activity against breast cancer. The individual isoforms are not available commercially, but Repros Therapeutics (The Woodlands, TX, USA) has separated them and is using enclomiphene citrate (ENC) in clinical trials in men with secondary hypogonadism who wish to preserve their fertility. Zuclomiphene, possessing no oestrogen antagonism at physiological concentrations, appears to have a longer biological half-life than enclomiphene, and thus may persist for long periods in the body. At high concentrations zuclomiphene can act as an oestrogen agonist. Clomiphene citrate (CC) is often used ‘off-label’ in men who have low testosterone to raise levels, it is also useful for the restoration of sperm counts in men. CC is approved by FDA and widely used in women for induction of ovulation for several conditions. CC is a mixture of two diastereoisomers, a cis isomer, zuclomiphene citrate (ZUC, 38%) and a trans isomer, ENC (62%). The two clomiphene isomers have mixed estrogenic and antiestrogenic effects that vary among species.

Ranitidine, a histamine H2-receptor antagonist, is now well established as a potent inhibitor of gastric acid secretion effective in the treatment and prophylaxis of gastrointestinal lesions aggravated by gastric acid secretion.

Tamoxifen (brand name Nolvadex), is selective estrogen receptor modulators (SERM) with tissue-specific activities for the treatment and prevention of estrogen receptor positive breast cancer. Tamoxifen itself is a prodrug, having relatively little affinity for its target protein, the estrogen receptor (ER). It is metabolized in the liver by the cytochrome P450 isoform CYP2D6 and CYP3A4 into active metabolites such as 4-hydroxytamoxifen (4-OHT) (afimoxifene) and N-desmethyl-4-hydroxytamoxifen (endoxifen) which have 30–100 times more affinity with the ER than tamoxifen itself. These active metabolites compete with estrogen in the body for binding to the ER. In breast tissue, 4-OHT acts as an ER antagonist so that transcription of estrogen-responsive genes is inhibited. Tamoxifen has 7% and 6% of the affinity of estradiol for the ERα and ERβ, respectively, whereas 4-OHT has 178% and 338% of the affinity of estradiol for the ERα and ERβ. The prolonged binding of tamoxifen to the nuclear chromatin of these results in reduced DNA polymerase activity, impaired thymidine utilization, blockade of estradiol uptake, and decreased estrogen response. It is likely that tamoxifen interacts with other coactivators or corepressors in the tissue and binds with different estrogen receptors, ER-alpha or ER-beta, producing both estrogenic and antiestrogenic effects. Tamoxifen is currently used for the treatment of both early and advanced estrogen receptor (ER)-positive (ER+) breast cancer in pre- and post-menopausal women. Additionally, it is the most common hormone treatment for male breast cancer. Patients with variant forms of the gene CYP2D6 (also called simply 2D6) may not receive full benefit from tamoxifen because of too slow metabolism of the tamoxifen prodrug into its active metabolites. Tamoxifen is used as a research tool to trigger tissue-specific gene expression in many conditional expression constructs in genetically modified animals including a version of the Cre-Lox recombination technique. Tamoxifen has been shown to be effective in the treatment of mania in patients with bipolar disorder by blocking protein kinase C (PKC), an enzyme that regulates neuron activity in the brain. Researchers believe PKC is over-active during the mania in bipolar patients.

Gallium citrate Ga 67 is the citrate salt of the radioisotope gallium Ga 67. Although the mechanism is unknown, gallium Ga 67 concentrates in lysosomes and is bound to a soluble intracellular protein in certain viable primary and metastatic tumors and focal sites of inflammation, allowing scintigraphic localization. Ga-67 scintigraphy (GS) cannot differentiate between tumor and acute inflammation. Gallium Citrate Ga 67 Injection may be useful in demonstrating the presence of the following malignancies: Hodgkins disease, lymphomas and bronchogenic carcinoma. Positive Ga 67 uptake in the absence of prior symptoms warrants follow-up as an indication of a potential disease state.

Lithium is an alkali metal widely used in industry. Lithium salts are indicated in the treatment of manic episodes of Bipolar Disorder. The use of lithium in psychiatry goes back to the mid-19th century. Early work, however, was soon forgotten, and John Cade is credited with reintroducing lithium to psychiatry for mania in 1949. Mogens Schou undertook a randomly controlled trial for mania in 1954, and in the course of that study became curious about lithium as a prophylactic for depressive illness. In 1970, the United States became the 50th country to admit lithium to the marketplace. The specific mechanisms by which lithium exerts its mood-stabilizing effects are not well understood. Lithium appears to preserve or increase the volume of brain structures involved in emotional regulation such as the prefrontal cortex, hippocampus and amygdala, possibly reflecting its neuroprotective effects. At a neuronal level, lithium reduces excitatory (dopamine and glutamate) but increases inhibitory (GABA) neurotransmission; however, these broad effects are underpinned by complex neurotransmitter systems that strive to achieve homeostasis by way of compensatory changes. For example, at an intracellular and molecular level, lithium targets second-messenger systems that further modulate neurotransmission. For instance, the effects of lithium on the adenyl cyclase and phospho-inositide pathways, as well as protein kinase C, may serve to dampen excessive excitatory neurotransmission. In addition to these many putative mechanisms, it has also been proposed that the neuroprotective effects of lithium are key to its therapeutic actions. In this regard, lithium has been shown to reduce the oxidative stress that occurs with multiple episodes of mania and depression. Further, it increases protective proteins such as brain-derived neurotrophic factor and B-cell lymphoma 2, and reduces apoptotic processes through inhibition of glycogen synthase kinase 3 and autophagy.