Like other thiazides, chlorothiazide promotes water loss from the body (diuretics). It inhibits Na /Cl- reabsorption from the distal convoluted tubules in the kidneys. Thiazides also cause loss of potassium and an increase in serum uric acid. Thiazides are often used to treat hypertension, but their hypotensive effects are not necessarily due to their diuretic activity. Thiazides have been shown to prevent hypertension-related morbidity and mortality although the mechanism is not fully understood. Thiazides cause vasodilation by activating calcium-activated potassium channels (large conductance) in vascular smooth muscles and inhibiting various carbonic anhydrases in vascular tissue. Chlorothiazide affects the distal renal tubular mechanism of electrolyte reabsorption. At maximal therapeutic dosages, all thiazides are approximately equal in their diuretic efficacy. Chlorothiazide increases excretion of sodium and chloride in approximately equivalent amounts. Natriuresis may be accompanied by some loss of potassium and bicarbonate. After oral doses, 10-15 percent of the dose is excreted unchanged in the urine. Chlorothiazide crosses the placental but not the blood-brain barrier and is excreted in breast milk. As a diuretic, chlorothiazide inhibits active chloride reabsorption at the early distal tubule via the Na-Cl cotransporter, resulting in an increase in the excretion of sodium, chloride, and water. Thiazides like chlorothiazide also inhibit sodium ion transport across the renal tubular epithelium through binding to the thiazide sensitive sodium-chloride transporter. This results in an increase in potassium excretion via the sodium-potassium exchange mechanism. The antihypertensive mechanism of chlorothiazide is less well understood although it may be mediated through its action on carbonic anhydrases in the smooth muscle or through its action on the large-conductance calcium-activated potassium (KCa) channel, also found in the smooth muscle. It is marketed under the brand name Diuril.

Amphotericin B used to treat progressive, potentially life-threatening fungal infections, such as oral thrush, vaginal candidiasis and esophageal candidiasis in patients with normal neutrophil counts. Also, Amphotericin B is often used in otherwise-untreatable protozoan infections such as visceral leishmaniasis and primary amoebic meningoencephalitis. As with other polyene antifungals, amphotericin B binds with ergosterol, a component of fungal cell membranes, forming a transmembrane channel that leads to monovalent ion (K+, Na+, H+ and Cl−) leakage, which is the primary effect leading to fungal cell death. When administered concurrently, the following drugs may interact with amphotericin B: Antineoplastic agents, Corticosteroids and Corticotropin (ACTH); Digitalis glycosides; Flucytosine; Imidazoles (e.g., ketoconazole, miconazole, clotrimazole, fluconazole, etc.); Zidovudine; Skeletal muscle relaxants (tubocurarine); Rifabutin; Leukocyte transfusions. The adverse reactions most commonly observed are: fever; malaise; weight loss; hypotension; tachypnea; anorexia; nausea; vomiting; diarrhea; dyspepsia; cramping epigastric pain; normochromic, normocytic anemia; pain at the injection site with or without phlebitis or thrombophlebitis; generalized pain, including muscle and joint pains; headache; decreased renal function and renal function abnormalities.

Perphenazine is a relatively high potency phenothiazine that blocks dopamine 2 receptors predominantly, but also may possess antagonist actions at histamine 1 and cholinergic M1 and alpha 1 adrenergic receptors in the vomiting center leading to reduced nausea and vomiting. The drug was approved by FDA for the treatment of schizophrenia and control of severe nausea and vomiting (either alone or in combination with amitriptyline hydrochloride). Perphenazine is extensively hepatic to metabolites via sulfoxidation, hydroxylation, dealkylation, and glucuronidation; primarily metabolized by CYP2D6 to N-dealkylated perphenazine, perphenazine sulfoxide, and 7-hydroxyperphenazine (active metabolite with 70% of the activity of perphenazine) and excreted in the urine and feces.

Prochlorperazine is a piperazine phenothiazine antipsychotic which block postsynaptic mesolimbic dopaminergic receptors in the brain and has antiemetic effects by its antagonist actions in the D2 dopamine receptors in the chemoreceptor trigger zone. It also exhibits alpha-adrenergic blocking effect on α1 receptros and may depress the release of hypothalamic and hypophyseal hormones. Prochlorperazine is used for the control of severe nausea and vomiting, for the treatment of schizophrenia. Prochlorperazine is effective for the short-term treatment of generalized non-psychotic anxiety. Prochlorperazine may be an effective treatment of acute headaches and refractory chronic daily headache.

Dapsone was synthesized in 1908 by Fromm and Wittmann. The drug was approved by FDA for the treatment of such conditions as acne vulgaris, leprosy and dermatitis herpetiformis, also the drug is used off-label for many skin diseases. Although the exact mechanism of dapsone action is unknown, it is speculated that it acts as both anti-inflammatory and antimicrobial agent. It was demonstrated that dapsone suppresses ROS generation, inhibits neutrophil myeloperoxidase and eosinophil peroxidase and also inhibits bacterial dihydropteroate synthase.

Chloroprocaine (Nesacaine®, Nesacaine®-MPF) is a non pyrogenic local anesthetic. Nesacaine® is indicated for the production of local anesthesia by infiltration and peripheral nerve block. It is not to be used for lumbar or caudal epidural anesthesia. Nesacaine®-MPF is indicated for the production of local anesthesia by infiltration, peripheral and central nerve block, including lumbar and caudal epidural blocks. Nesacaine® and Nesacaine®-MPF are not to be used for subarachnoid administration. Chloroprocaine (Nesacaine®, Nesacaine®-MPF), like other local anesthetics, blocks the generation and the conduction of nerve impulses, presumably by increasing the threshold for electrical excitation in the nerve, by slowing the propagation of the nerve impulse and by reducing the rate of rise of the action potential. It acts mainly by inhibiting sodium influx through voltage gated sodium channels in the neuronal cell membrane of peripheral nerves. When the influx of sodium is interrupted, an action potential cannot arise and signal conduction is thus inhibited.

Chlorpromazine is a psychotropic agent indicated for the treatment of schizophrenia. It also exerts sedative and antiemetic activity. Chlorpromazine has actions at all levels of the central nervous system-primarily at subcortical levels-as well as on multiple organ systems. Chlorpromazine has strong antiadrenergic and weaker peripheral anticholinergic activity; ganglionic blocking action is relatively slight. It also possesses slight antihistaminic and antiserotonin activity. Chlorpromazine acts as an antagonist (blocking agent) on different postsysnaptic receptors -on dopaminergic-receptors (subtypes D1, D2, D3 and D4 - different antipsychotic properties on productive and unproductive symptoms), on serotonergic-receptors (5-HT1 and 5-HT2, with anxiolytic, antidepressive and antiaggressive properties as well as an attenuation of extrapypramidal side-effects, but also leading to weight gain, fall in blood pressure, sedation and ejaculation difficulties), on histaminergic-receptors (H1-receptors, sedation, antiemesis, vertigo, fall in blood pressure and weight gain), alpha1/alpha2-receptors (antisympathomimetic properties, lowering of blood pressure, reflex tachycardia, vertigo, sedation, hypersalivation and incontinence as well as sexual dysfunction, but may also attenuate pseudoparkinsonism - controversial) and finally on muscarinic (cholinergic) M1/M2-receptors (causing anticholinergic symptoms like dry mouth, blurred vision, obstipation, difficulty/inability to urinate, sinus tachycardia, ECG-changes and loss of memory, but the anticholinergic action may attenuate extrapyramidal side-effects). Additionally, Chlorpromazine is a weak presynaptic inhibitor of Dopamine reuptake, which may lead to (mild) antidepressive and antiparkinsonian effects. Chlorpromazine has being marketed under the trade names Thorazine and Largactil among others. Chlorpromazine is used for treating certain mental or mood disorders (eg, schizophrenia), the manic phase of manic-depressive disorder, anxiety and restlessness before surgery, the blood disease porphyria, severe behavioral and conduct disorders in children, nausea and vomiting, and severe hiccups.

Furadantin (nitrofurantoin), a synthetic chemical, is a stable, yellow, crystalline compound. Furadantin is an antibacterial agent for specific urinary tract infections. Orally administered Furadantin is readily absorbed and rapidly excreted in urine. Blood concentrations at therapeutic dosage are usually low. Unlike many drugs, the presence of food or agents delaying gastric emptying can increase the bioavailability of Furadantin, presumably by allowing better dissolution in gastric juices. Nitrofurantoin is active against some gram positive organisms such as S. aureus, S. epidermidis, S. saprophyticus, Enterococcus faecalis, S. agalactiae, group D streptococci, viridians streptococci and Corynebacterium. Its spectrum of activity against gram negative organisms includes E. coli, Enterobacter, Neisseria, Salmonella and Shigella. It may be used as an alternative to trimethoprim/sulfamethoxazole for treating urinary tract infections though it may be less effective at eradicating vaginal bacteria. May also be used in females as prophylaxis against recurrent cystitis related to coitus. Nitrofurantoin is highly stable to the development of bacterial resistance, a property thought to be due to its multiplicity of mechanisms of action. Nitrofurantoin is activated by bacterial flavoproteins (nitrofuran reductase) to active reduced reactive intermediates that are thought to modulate and damage ribosomal proteins or other macromolecules, especially DNA, causing inhibition of DNA, RNA, protein, and cell wall synthesis. The overall effect is inhibition of bacterial growth or cell death.

Erythromycin cyclocarbonate (Davercin) is a first generation semi-synthetic erythromycin. It is active against Gram-positive and some Gram-negative microorganisms. Davercin shows comparable or better in vitro potency, low host toxicity and improved pharmacokinetics compared with erythromycin. It is approved for the treatment of acne, atypical pneumonia (caused by Mycoplasma pneumoniae, Chlamydia pneumoniae, Legionella pneumophila), whooping cough (treatment and prevention), urethritis (caused by Ureaplasma urealyticum and Chlamydia trachomatis), gastrointestinal infection caused by Campylobacter spp., short-term infections of the skin and soft tissues (e.g. acne, staphylococcal dermatitis). In streptococcal infections, diphtheria, gonorrhea, early syphilis in patients who are allergic to penicillin, and in the prevention of bacterial endocarditis before the planned dental procedures. Adverse effects are: nausea, vomiting, abdominal pain, diarrhea, skin allergic reactions.

Promethazine is a phenothiazine derivative with histamine H1-blocking, antimuscarinic, and sedative properties. Promethazine HCl Oral Solution is useful for: perennial and seasonal allergic rhinitis. Allergic conjunctivitis due to inhalant allergens and foods. Anaphylactic reactions, as adjunctive therapy to epinephrine and other standard measures, after the acute manifestations have been controlled. Preoperative, postoperative, or obstetric sedation. Prevention and control of nausea and vomiting associated with certain types of anesthesia and surgery. Therapy adjunctive to meperidine or other analgesics for control of post-operative pain. Active and prophylactic treatment of motion sickness. Antiemetic therapy in postoperative patients.