Niacinamide, known as nicotinamide, is an important compound functioning as a component of the coenzyme NAD. Its primary significance is in the prevention and/or cure of blacktongue and pellagra. Pellagra is a nutritional disease that occurs due to insufficient dietary amounts of vitamin B3 or the chemical it is made from (tryptophan). Symptoms of pellagra include skin disease, diarrhea, dementia, and depression. In addition, was experiments, revealed, that niacinamide hydroiodide might have role in ophthalmology and parenteral use of niacinamide hydroiodide can treat arteriosclerotic syndromes.

Iodide ion I-123 is the most suitable isotope of iodine for the diagnostic study of thyroid diseases. Sodium Iodide I 131 Capsules Diagnostic is indicated for use in adults for: Assessment of thyroid function using radioactive iodine (RAI) uptake test and Imaging the thyroid (scintigraphy). The following adverse reaction has been described elsewhere in the labeling: Hypersensitivity Reactions. The following adverse reactions have been identified during post-approval use from Sodium Iodide I 131 Capsules Diagnostic: Gastrointestinal disorders (vomiting, nausea, and diarrhea); General disorders and administration site conditions (local thyroid swelling); Immune system disorders (hypersensitivity reactions); Skin and subcutaneous tissue disorders (itching, rash, hives, and erythema). Certain drugs and iodine-containing foods interfere with the accumulation of radioiodide by the thyroid.

Iodide ion I-125 is radioisotope of iodine with half-life 59.4 days. It decays with the emission of low-energy gamma rays. It is used as a source for bone densitometry devices, protein iodination. Seeds implantations with I-125 are used in the clinics for the treatment of prostate cancer, malignant biliary obstruction, non-small cell lung cancer, colorectal cancer, uveal melanoma, and other tumors.

Iodide I-131 (as Sodium iodide I-131) is a radioisotopic drug used for the treatment and palliation of thyroid malignancy. Therapeutic solutions of Sodium Iodide-131 are indicated for the treatment of hyperthyroidism and thyroid carcinomas that take up iodine. Palliative effects may be observed in patients with advanced thyroid malignancy if the metastatic lesions take up iodine. It is also indicated for use in performance of the radioactive iodide (RAI) uptake test to evaluate thyroid function. Taken orally, sodium iodide I-131 is rapidly absorbed and distributed within the extracellular fluid of the body. The iodide is concentrated in the thyroid via the sodium/iodide symporter, and subsequently oxidized to iodine. The destruction of thyroidal tissue is achieved by the beta emission of sodium iodide I-131.

Ascorbic acid (vitamin C) is a water-soluble vitamin. It occurs as a white or slightly yellow crystal or powder with a slight acidic taste. Ascorbic acid is an electron donor, and this property accounts for all its known functions. As an electron donor, ascorbic acid is a potent water-soluble antioxidant in humans. Ascorbic acid acts as an antioxidant under physiologic conditions exhibiting a cross over role as a pro-oxidant in pathological conditions. Oxidized ascorbic acid (dehydroascorbic acid (DHA) directly inhibits IkappaBalpha kinase beta (IKKbeta) and IKKalpha enzymatic activity in vitro, whereas ascorbic acid did not have this effect. These findings define a function for vitamin C in signal transduction other than as an antioxidant and mechanistically illuminate how vitamin C down-modulates NF-kappaB signaling. Vitamin C is recommended for the prevention and treatment of scurvy. Its parenteral administration is desirable for patients with an acute deficiency or for those whose absorption of orally ingested ascorbic acid (vitamin c) is uncertain. Symptoms of mild deficiency may include faulty bone and tooth development, gingivitis, bleeding gums, and loosened teeth. Febrile states, chronic illness, and infection (pneumonia, whooping cough, tuberculosis, diphtheria, sinusitis, rheumatic fever, etc.) increase the need for ascorbic acid (vitamin c). Hemovascular disorders, burns, delayed fracture and wound healing are indications for an increase in the daily intake.

Niacin (also known as vitamin B3 and nicotinic acid) is bio converted to nicotinamide which is further converted to nicotinamide adenine dinucleotide (NAD+) and the hydride equivalent (NADH) which are coenzymes necessary for tissue metabolism, lipid metabolism, and glycogenolysis. Niacin (but not nicotinamide) in gram doses reduces LDL-C, Apo B, Lp(a), TG, and TC, and increases HDL-C. The increase in HDL-C is associated with an increase in apolipoprotein A-I (Apo A-I) and a shift in the distribution of HDL subfractions. These shifts include an increase in the HDL2:HDL3 ratio, and an elevation in lipoprotein A-I (Lp A-I, an HDL-C particle containing only Apo A-I). The mechanism by which niacin alters lipid profiles is not completely understood and may involve several actions, including partial inhibition of release of free fatty acids from adipose tissue, and increased lipoprotein lipase activity (which may increase the rate of chylomicron triglyceride removal from plasma). Niacin decreases the rate of hepatic synthesis of VLDL-C and LDL-C, and does not appear to affect fecal excretion of fats, sterols, or bile acids. As an adjunct to diet, the efficacy of niacin and lovastatin in improving lipid profiles (either individually, or in combination with each other, or niacin in combination with other statins) for the treatment of dyslipidemia has been well documented. The effect of combined therapy with niacin and lovastatin on cardiovascular morbidity and mortality has not been determined. In addition, preliminary reports suggest that niacin causes favorable LDL particle size transformations, although the clinical relevance of this effect is not yet clear. April 15, 2016: Based on several large cardiovascular outcome trials including AIM-HIGH, ACCORD, and HPS2-THRIVE, the FDA decided that "scientific evidence no longer supports the conclusion that a drug-induced reduction in triglyceride levels and/or increase in HDL-cholesterol levels in statin-treated patients results in a reduction in the risk of cardiovascular events" Consistent with this conclusion, the FDA has determined that the benefits of niacin ER tablets for coadministration with statins no longer outweigh the risks, and the approval for this indication should be withdrawn.

Trigonellamide (1-Methylnicotinamide) is a metabolite of nicotinamide and is produced primarily in the liver by nicotinamide N-methyltransferase. Trigonellamide may be an endogenous activator of prostacyclin (PGI2) production and thus may regulate thrombotic as well as inflammatory processes in the cardiovascular system. The mechanisms of action of Trigonellamide involve the activation of PGI2 release driven by cyclooxygenase 2 (COX-2). PGI2 releasing capacity of 1- Trigonellamide was shown to afford not only anti-thrombotic but also fibrinolytic, anti-inflammatory and gastroprotective effects. Interestingly, Trigonellamide did not directly either affect the activity of leucocytes or release PGI2 in the perfused rat hindquarters model. Still, Trigonellamide, due to its PGI2 releasing capacity, might serve as a hepatoprotective agent that protects against Concanavalin-A induced liver injury through the downregulation of interleukin-4 (IL-4) and tumor necrosis factor-α signalization (TNF-α). In addition to its anti-platelet, anti-thrombotic and anti-inflammatory activities, 1-MNA has also been shown to restore endothelial function in diabetic hyperglycemic rats, as well as to improve endothelial function in humans. PGI2 displays anti-metastatic activity, and the PGI2 releasing activity of Trigonellamide, the potential application of exogenous Trigonellamide to prevent metastatic cancer.