Coumarin itself was first isolated from the tonka bean Coumarouna odorata. Coumarin and its derivatives are alpha-benzopyrones. Coumarin is metabolized in humans to 7-hydroxycoumarin. Coumarin is a secondary phytochemical with hepatotoxic and carcinogenic properties. For the carcinogenic effect, a genotoxic mechanism was considered possible. Coumarins have a significant effect on physiological, bacteriostatic and anti-tumor activity. Coumarins have potent edema protective function and thus involved in the treatment of lymphedema, elephantiasis and other high protein edema conditions. Coumarin has appetite-suppressing properties.

Quinine valerate is a salt of anti-malarial alkaloid quinine. Quinine valerate is considered to exert the same anti-malarial activity as the parent compound. Quinine valerate may be mutagenic in E. coli HCR+ strains.

Hesperidin is a flavanone glycoside found in citrus fruits. Its aglycone form is called hesperetin. Its name is derived from the word "hesperidium", for fruit produced by citrus trees. Hesperidin was first isolated in 1828 by French chemist Lebreton from the white inner layer of citrus peels (mesocarp, albedo). As a flavanone found in citrus fruits (such as oranges, lemons or pummelo fruits), hesperidin is under laboratory research for possible biological properties. One area of research is focused on the possible chemopreventive effects of hesperidin, but there is no current proof that hesperidin has this role in human cancer mechanisms. Hesperidin was effective in an animal model of Alzheimer's, alleviating pathological changes induced by aluminum. Early research suggests that taking one tablet of a specific product (Daflon 500, Les Laboratoires Servier) containing hesperidin and diosmin by mouth for 45 days decreases blood sugar levels and improves blood sugarcontrol in women with type 2 diabetes. For Rheumatoid arthritis (RA): early research suggests that drinking a beverage containing alpha-glucosyl hesperidin for 12 weeks improves symptoms of RA. Orally, hesperidin can cause gastrointestinal side effects, including abdominal pain, diarrhea, and gastritis. Headache can also occur in some patients. The possible anti-inflammatory action of hesperidin is probably due to the possible anti-inflammatory action of its aglycone hesperetin. Hesperetin appears to interfere with the metabolism of arachidonic acid as well as with histamine release. Hesperetin appears to inhibit phospholipase A2, lipoxygenase and cyclo-oxygenase. There is evidence that hesperetin inhibits histamine release from mast cells, which would account for the possible anti-allergic activity of hesperidin. The possible hypolipidemic effect of hesperidin is probably due to hesperetin's possible action in lipid lowering. Hesperetin may reduce plasma cholesterol levels by inhibition of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, as well as acyl coenzyme A: cholesterol acytransferase (ACAT). Inhibition of these enzymes by hesperetin has been demonstrated in rats fed a high cholesterol diet. The mechanism of hesperidin's possible vasoprotective action is unclear. Animal studies have shown that hesperidin decreases microvascular permeability. Hesperidin, itself or via hesperetin, may protect endothelial cells from hypoxia by stimulating certain mitochondrial enzymes, such as succinate dehydrogenase. The mechanism of hesperidin's possible anticarcinogenic action is also unclear. One explanation may be the inhibition of polyamine synthesis. Inhibition of lipoxygenase and cyclo-oxygenase is another possibility.

Pelletierine is an alkaloid found in the root-bark of the pomegranate tree. There is a little information about the pharmacological application of this compound, but one article describes the anthelminthic activity of pelletierine.

Ferric (III) salicylate is a product, formed when iron (III) ions react with salicylates. The presence of ferric salicylate gives a solution a characteristic purple color, and is used for rapid determination of salicylic acid and its metabolites in plasma and urine.

Acetone (or propanone) is the smallest and simplest ketone, which is used in cosmetic as a nail polish remover. Acetone is produced within the body because of the breakdown of stored fats and lipids as a source of energy. Such conditions as physical exercise and prolonged dieting, which lead to cleavage of fat within the body, may result in higher than average amounts of acetone in the bloodstream. The concentration of acetone in the environment doesn’t cause a neurotoxic, carcinogenic, or reproductive health hazard effect. In addition, experiments on rodents have shown that acetone possesses anticonvulsant properties.

Cinchonine is cinchona bark alkaloid, which was used to treat malaria. Cinchonine is more efficient than quinine in increasing the intracellular accumulation and restoring the cytotoxicity of doxorubicin, mitoxantrone and vincristine on well-characterized multidrug resistance (MDR) cell lines. In the phase I of clinical trial was investigated the properties of cinchonine combined with the CHVP (cyclophosphamide, doxorubicin, vinblastine, methylprednisolone) regimen in relapsed and refractory lymphoproliferative syndromes.

Ethylmorphine is a derivative of morphine with analgesic and antitussive effect. It acts by activating the opioid receptors and thus has a direct influence on the CNS system. Ethylmorphine was approved in Europe for the treatment of dry cough (Codethyline, Dionine).

Cevadine, veratridine, and related lipophilic ceveratrum alkaloids cause activation of the voltage-sensitive Na+ channels of nerve, heart, and skeletal muscle cell membranes similar to pyrethrins. Both veratridine and cevadine alter the ion selectivity of Na+ channels and cause persistent activation. The receptor for these alkaloids has not been isolated, but experiments indicate it is distinct from that of pyrethrin. Structurally, veratridine and cevadine differ only in their acyl group. Cevadine has been used as an insecticide, acting as a paralytic agent with higher toxicity to insects than to mammals. It has been used to study Na+ channel blockers such as vincamine and vincanol by inducing Na+ channels in the presence and absence of the drugs being tested.