Phenylpropanolamine belongs to the sympathomimetic amine class of drugs and is structurally related to ephedrine. The effects of phenylpropanolamine are largely the result of alpha-adrenergic agonist activity resulting from both direct stimulation of adrenergic receptors and release of neuronal norepinephrine. Phenylpropanolamine is mainly used as a nasal decongestant. Phenylpropanolamine is also used as anorexiant in obesity and to treat urinary incontinence in veteranary. Phenylpropanolamine containing products has been withdrawn by FDA due to the association of phenylpropanolamine use with increased risk of hemorrhagic stroke.

Phenylpropanolamine belongs to the sympathomimetic amine class of drugs and is structurally related to ephedrine. The effects of phenylpropanolamine are largely the result of alpha-adrenergic agonist activity resulting from both direct stimulation of adrenergic receptors and release of neuronal norepinephrine. Phenylpropanolamine is mainly used as a nasal decongestant. Phenylpropanolamine is also used as anorexiant in obesity and to treat urinary incontinence in veteranary. Phenylpropanolamine containing products has been withdrawn by FDA due to the association of phenylpropanolamine use with increased risk of hemorrhagic stroke.

Phenylpropanolamine belongs to the sympathomimetic amine class of drugs and is structurally related to ephedrine. The effects of phenylpropanolamine are largely the result of alpha-adrenergic agonist activity resulting from both direct stimulation of adrenergic receptors and release of neuronal norepinephrine. Phenylpropanolamine is mainly used as a nasal decongestant. Phenylpropanolamine is also used as anorexiant in obesity and to treat urinary incontinence in veteranary. Phenylpropanolamine containing products has been withdrawn by FDA due to the association of phenylpropanolamine use with increased risk of hemorrhagic stroke.

2,4-dinitrophenol (DNP) is a FDA-banned weight-loss agent and EPA-regulated environmental toxicant, traditionally used in research labs as an uncoupler of OXPHOS. Although not licensed for human consumption, DNP and DNP crystal form are used by bodybuilders and extreme dieters for their fat burning properties through inhibiting efficient energy (ATP) production in cells. Through uncoupling mitochondrial oxidative phosphorylation by facilitating proton transport across the mitochondrial membrane, DNP leads to rapid consumption of energy without generating ATP and consequently, to increased fat metabolism. However, the weight-loss effect comes with serious, and in some cases potentially fatal, adverse side effects, namely hyperthermia (the leading cause of fatality with acute DNP toxicity) and cardiac arrest, but also diaphoresis, tachycardia, tachypnea, skin toxicity, Fourier’s gangrene and cataracts with low dose chronic exposure. The proposed mechanism of DNP induced toxicity suggests the activation of ATP-sensitive K+ channels.

Oxedrine (Sympatol, p-synephrine) is a naturally occurring alkaloid molecule first appeared in Europe towards the end of the 1920s being sold as a drug under the brand name Sympatol. Oxedrine was then being prescribed as a remedy for a number of respiratory conditions, which include asthma, whooping cough, colds, and hay fever. More recently, synephrine gained popularity as a weight loss aid and it has become a favored component in the more popular brands of weight loss supplement stacks. This popularity can be attributed in part to the ban imposed on ephedra, to which it shares similar mechanisms of action. Most, if not all of the synephrine being sold as a dietary supplement is extracted and synthesized from the Citrus aurantium plant, more commonly known as bitter orange. Just like ephedrine, synephrine has vasoconstrictive abilities, although at a lesser potency compared to ephedrine. There is no mention of synephrine in editions of Drill's Pharmacology in Medicine later than the 3rd, nor is there any reference to synephrine in the 2012 Physicians' Desk Reference, nor in the current FDA "Orange Book". One current reference source describes synephrine as a vasoconstrictor that has been given to hypotensive patients, orally or by injection, in doses of 20–100 mg.

Oxedrine (Sympatol, p-synephrine) is a naturally occurring alkaloid molecule first appeared in Europe towards the end of the 1920s being sold as a drug under the brand name Sympatol. Oxedrine was then being prescribed as a remedy for a number of respiratory conditions, which include asthma, whooping cough, colds, and hay fever. More recently, synephrine gained popularity as a weight loss aid and it has become a favored component in the more popular brands of weight loss supplement stacks. This popularity can be attributed in part to the ban imposed on ephedra, to which it shares similar mechanisms of action. Most, if not all of the synephrine being sold as a dietary supplement is extracted and synthesized from the Citrus aurantium plant, more commonly known as bitter orange. Just like ephedrine, synephrine has vasoconstrictive abilities, although at a lesser potency compared to ephedrine. There is no mention of synephrine in editions of Drill's Pharmacology in Medicine later than the 3rd, nor is there any reference to synephrine in the 2012 Physicians' Desk Reference, nor in the current FDA "Orange Book". One current reference source describes synephrine as a vasoconstrictor that has been given to hypotensive patients, orally or by injection, in doses of 20–100 mg.

Oxedrine (Sympatol, p-synephrine) is a naturally occurring alkaloid molecule first appeared in Europe towards the end of the 1920s being sold as a drug under the brand name Sympatol. Oxedrine was then being prescribed as a remedy for a number of respiratory conditions, which include asthma, whooping cough, colds, and hay fever. More recently, synephrine gained popularity as a weight loss aid and it has become a favored component in the more popular brands of weight loss supplement stacks. This popularity can be attributed in part to the ban imposed on ephedra, to which it shares similar mechanisms of action. Most, if not all of the synephrine being sold as a dietary supplement is extracted and synthesized from the Citrus aurantium plant, more commonly known as bitter orange. Just like ephedrine, synephrine has vasoconstrictive abilities, although at a lesser potency compared to ephedrine. There is no mention of synephrine in editions of Drill's Pharmacology in Medicine later than the 3rd, nor is there any reference to synephrine in the 2012 Physicians' Desk Reference, nor in the current FDA "Orange Book". One current reference source describes synephrine as a vasoconstrictor that has been given to hypotensive patients, orally or by injection, in doses of 20–100 mg.

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.

Elaidic acid is the 9-trans isomer of oleic acid. It is a monounsaturated trans-fatty acid, which can be found in partially hydrogenated cooking oils. It was revealed, that elaidic acid inhibits HHT and HETE formation in human platelets incubated with arachidonic acid. Also was shown, that trans oleic acid increased plasma CETP activity, which increases low-density lipoprotein (LDL) cholesterol and decreases high-density lipoprotein (HDL).

Elaidic acid is the 9-trans isomer of oleic acid. It is a monounsaturated trans-fatty acid, which can be found in partially hydrogenated cooking oils. It was revealed, that elaidic acid inhibits HHT and HETE formation in human platelets incubated with arachidonic acid. Also was shown, that trans oleic acid increased plasma CETP activity, which increases low-density lipoprotein (LDL) cholesterol and decreases high-density lipoprotein (HDL).