Quinethazone (brand name Hydromox) is a thiazide diuretic used to treat hypertension. The antihypertensive mechanism of quinethazone is less well understood. This drug was discovered in a period when only isoform carbonic anhydrases (CAs) II was known and considered physiologically/pharmacologically relevant. Recently was studied that quinethazone considerably inhibit other isozymes known nowadays to be involved in critical physiologic processes. Thiazides like quinethazone also inhibit sodium ion transport across the renal tubular epithelium through binding to the thiazide sensitive sodium-chloride transporter. Common side effects include dizziness, dry mouth, nausea, and low potassium levels. Thiazides may increase the toxicity of allopurinol, anesthetics, antineoplastic, calcium salts, diazoxide, digitalis, lithium; loop diuretics, methyldopa, nondepolarizing muscle relaxants, vitamin D; amphotericin B and anticholinergics may increase the toxicity of thiazides.

Sulfaphenazole is an oral antibiotic, which was used for the treatment of bacterial infections under the name Sulfabid. The drug was found to block folate synthesis in bacterias by inhibiting the enzyme dihydropteroate synthase. Sulfaphenazole is also known to inhibit CYP2C9 with high potency and specificity. Sulfabid is no longer marketed in the USA.

Idoxuridine is an antiviral agent use in keratitis caused by herpes simplex virus. As a prescription drug it comes as a 0.1% ophthalmic solution/drops (Herplex and Dendrid). The first studies of the compound for treatment of human herpes simplex started in early 1960s. Being a structural analog of thymidine idoxuridine inhibits viral DNA replication by substituting thymidine. The effect of idoxuridine results in the inability of the virus to reproduce and/or infect tissues. Idoxuridine also blocks viral thymidine kinase as its substrate analog.

Dydrogesterone is an orally active progestogen which acts directly on the uterus, producing a complete secretory endometrium in an estrogen-primed uterus. At therapeutic levels, dydrogesterone has no contraceptive effect as it does not inhibit or interfere with ovulation or the corpus luteum. Furthermore, dydrogesterone is non-androgenic, non-estrogenic, non-corticoid, non-anabolic and is not excreted as pregnanediol. Dydrogesterone helps to regulate the healthy growth and normal shedding of the uterus lining. Therefore, it may be useful in the treatment of menstrual disorders such as absent, irregular or painful menstrual periods, infertility, premenstrual syndrome and endometriosis. Dydrogesterone works by regulating the healthy growth and normal shedding of the womb lining by acting on progesterone receptors in the uterus. Used to treat irregular duration of cycles and irregular occurrence and duration of periods caused by progesterone deficiency. Also used to prevent natural abortion in patients who have a history of habitual abortions. Dydrogesterone was first introduced to the market in 1961, and is currently approved in over 100 countries world-wide. Banned in the USA and wthdrawn from the UK, but still used in other countries.

Chlorprothixene (Taractan, Tarasan, Truxal) is a thioxanthine derivative developed by Lundbeck for the treatment of psychotic disorders. The drug exerts its activity by binding to and inhibiting serotonin receptors, dopamine receptors, muscarinic acetylcholine receptor, histamine H1 receptor and alpha1-adrenergic receptor.

Methysergide is an oral, synthetic ergot alkaloid, structurally related to the oxytocic agent methylergonovine and to the potent hallucinogen LSD. Methysergide is used prophylactically to reduce the frequency and intensity of severe vascular headaches. Although methysergide is an ergot alkaloid, it is a weak vasoconstrictor and oxytocic. Methysergide is a more potent antagonist of peripheral serotonin receptors than other ergot alkaloids. Methysergide is not just a 5HT2 antagonist, it is also a 5HT1 agonist. Although methysergide and sumatriptan both stimulate serotonin receptors centrally, methysergide is intended for prophylaxis while sumatriptan is indicated for treatment of an acute attack. Methysergide was approved by the FDA in 1962. Methysergide was formerly used for prophylaxis of cluster headaches/migraine headaches, but is no longer recommended due to retroperitoneal/retropulmonary fibrosis.

Stanozolol is a synthetic anabolic steroid derived from dihydrotestosterone. It is indicated prophylactically to decrease the frequency and severity of attacks of angioedema. In rare cases, serious and even fatal cases of liver problems have developed during treatment with stanozolol. Anabolic steroids may increase sensitivity to anticoagulants; therefore, dosage of an anticoagulant may have to be decreased in order to maintain the prothrombin time at the desired therapeutic level.

Iopanoic acid and ipodate salts have been used for oral cholangiography to visualize the biliary ducts. Ipodate salts have been used for the long-term treatment of Graves' disease and in hyperthyroidism. Ipodate reduced levels of T3 and T4 in the patients. Ipodate also inhibits the conversion of T4 to T3. It is not considered a first-line approach. Ipodate sodium lacks FDA approval for these uses. During investigation of mechanism of action was discovered, that binding of sodium ipodate with nuclear T3 receptors was not a prominent mechanism via which the drug attenuates T3 effects in vivo. Sodium ipodate could enhance T3 effects at the cellular level and that enhancement could not be reflected by routinely monitored serum TSH.

Iopydol is an X-ray contrast medium used in conjunction with iopydone as the proprietary preparation, Hytrast, for the bronchography.

Uramustine (INN) or uracil mustard is a chemotherapy drug which belongs to the class of alkylating agents. It is used in lymphatic malignancies such as non-Hodgkin's lymphoma. Uracil Mustard selectively inhibits the synthesis of deoxyribonucleic acid (DNA). The guanine and cytosine content correlates with the degree of Uracil Mustard-induced cross-linking. At high concentrations of the drug, cellular RNA and protein synthesis are also suppressed. After activation, it binds preferentially to the guanine and cytosine moieties of DNA, leading to cross-linking of DNA, thus inhibiting DNA synthesis and function. The DNA damage leads to apoptosis of the affected cells. Chemically it is a derivative of nitrogen mustard and uracil.