Penicillamine, sold under the trade names of Cuprimine among others, is a medication primarily used for treatment of Wilson's disease, cystinuria and active rheumatoid arthritis. Penicillamine is a chelating agent recommended for the removal of excess copper in patients with Wilson's disease. From in vitro studies which indicate that one atom of copper combines with two molecules of penicillamine. Penicillamine also reduces excess cystine excretion in cystinuria. This is done, at least in part, by disulfide interchange between penicillamine and cystine, resulting in formation of penicillamine-cysteine disulfide, a substance that is much more soluble than cystine and is excreted readily. Penicillamine interferes with the formation of cross-links between tropocollagen molecules and cleaves them when newly formed. The mechanism of action of penicillamine in rheumatoid arthritis is unknown although it appears to suppress disease activity. Unlike cytotoxic immunosuppressants, penicillamine markedly lowers IgM rheumatoid factor but produces no significant depression in absolute levels of serum immunoglobulins. Also unlike cytotoxic immunosuppressants which act on both, penicillamine in vitro depresses T-cell activity but not B-cell activity.

Quinine soluble salts possess the extremely bitter taste, that may have a perplexing problem especially to children. That is why the most common combinations which are administered in this way are the sulphate, salicylate, tannate and certain esters. Quinine tannate, an insoluble quinine salt has been known in medicine for a very long time. However, many experiments have revealed that quinine tannate was practically inert as a medicinal substance.

Phosphate is a major intracellular anion in mammals. Hydrogen phopshate is a protonated form of phosphate. In serum, phosphate exists in two forms, dihydrogen phosphate (H2PO4) and its salt, mono-hydrogen phosphate (HPO4). At the physiologic pH of 7.40, the pK of H2PO4 is 6.8 and the ratio of HPO4 to H2PO4 is 4:1. Altered level of phosphate can be an indicator of various disorders, such as chronic renal failure, hypoparathyroidism, familial intermittent hyperphosphatemia, endocrine disorders, hyperthyroidism, acromegaly, juvenile hypogonadism, etc. These disorders may lead to either hyper- or hypophosphatemia, which can be caused by cellular shifts of phosphate. Patients with hypophosphatemia can be treated with dietary phosphate supplements (potassium phosphate, for example).

Lidocaine is a local anesthetic and cardiac depressant used to numb tissue in a specific area and for management of cardiac arrhythmias, particularly those of ventricular origins, such as occur with acute myocardial infarction. Lidocaine alters signal conduction in neurons by blocking the fast voltage-gated Na+ channels in the neuronal cell membrane responsible for signal propagation. With sufficient blockage, the membrane of the postsynaptic neuron will not depolarize and will thus fail to transmit an action potential. This creates the anesthetic effect by not merely preventing pain signals from propagating to the brain, but by stopping them before they begin. Careful titration allows for a high degree of selectivity in the blockage of sensory neurons, whereas higher concentrations also affect other modalities of neuron signaling. Lidocaine exerts an antiarrhythmic effect by increasing the electrical stimulation threshold of the ventricle during diastole. In usual therapeutic doses, lidocaine hydrochloride produces no change in myocardial contractility, in systemic arterial pressure, or an absolute refractory period. The efficacy profile of lidocaine as a local anesthetic is characterized by a rapid onset of action and intermediate duration of efficacy. Therefore, lidocaine is suitable for infiltration, block, and surface anesthesia. Longer-acting substances such as bupivacaine are sometimes given preference for spinal and epidural anesthesias; lidocaine, though, has the advantage of a rapid onset of action. Lidocaine is also the most important class-1b antiarrhythmic drug; it is used intravenously for the treatment of ventricular arrhythmias (for acute myocardial infarction, digoxin poisoning, cardioversion, or cardiac catheterization) if amiodarone is not available or contraindicated. Lidocaine should be given for this indication after defibrillation, CPR, and vasopressors have been initiated. A routine preventative dose is no longer recommended after a myocardial infarction as the overall benefit is not convincing. Inhaled lidocaine can be used as a cough suppressor acting peripherally to reduce the cough reflex. This application can be implemented as a safety and comfort measure for patients who have to be intubated, as it reduces the incidence of coughing and any tracheal damage it might cause when emerging from anesthesia. Adverse drug reactions (ADRs) are rare when lidocaine is used as a local anesthetic and is administered correctly. Most ADRs associated with lidocaine for anesthesia relate to administration technique (resulting in systemic exposure) or pharmacological effects of anesthesia, and allergic reactions only rarely occur. Systemic exposure to excessive quantities of lidocaine mainly result in a central nervous system (CNS) and cardiovascular effects – CNS effects usually occur at lower blood plasma concentrations and additional cardiovascular effects present at higher concentrations, though cardiovascular collapse may also occur with low concentrations.

P-32 is a radioactive isotope of phosphorus with a half-life of 14.29 days. Radioactive decay of P-32 produces beta-particles (electrons) which are able to penetrate tissue at a range of 3-8 mm. Phosphate ion P-32 has many applications in medicine and biology. P32 sodium phosphate was approved by the FDA for the treatment of polycythemia vera, chronic myelocytic leukemia, and chronic lymphocytic leukemia. P32-phosphate may also be used in the palliative treatment of selected patients with multiple areas of skeletal metastases. As metabolic uptake of phosphorus is selectively increased in malignant tissues, P-32 was also used for cancer diagnostics.

Chloroquine (brand name Aralen) is indicated for the suppressive treatment and for acute attacks of malaria due to P. vivax, P.malariae, P. ovale, and susceptible strains of P. falciparum. The drug is also indicated for the treatment of extraintestinal amebiasis. In addition, chloroquine is in clinical trials as an investigational antiretroviral in humans with HIV-1/AIDS and as a potential antiviral agent against chikungunya fever. The mechanism of plasmodicidal action of chloroquine is not completely certain. However, is existed theory, that like other quinoline derivatives, it is thought to inhibit heme polymerase activity. The heme moiety consists of a porphyrin ring called Fe(II)-protoporphyrin IX (FP). To avoid destruction by this molecule, the parasite biocrystallizes heme to form hemozoin, a non-toxic molecule. Chloroquine enters the red blood cell, inhabiting parasite cell, and digestive vacuole by simple diffusion. Chloroquine then becomes protonated (to CQ2+), as the digestive vacuole is known to be acidic (pH 4.7); chloroquine then cannot leave by diffusion. Chloroquine caps hemozoin molecules to prevent further biocrystallization of heme, thus leading to heme buildup. Chloroquine binds to heme (or FP) to form what is known as the FP-Chloroquine complex; this complex is highly toxic to the cell and disrupts membrane function.