Aldioxa is the generic name for the metal complex, dihydroxyaluminum allantoinate, which is hydrolyzed to allantoin and aluminium hydrate at the gastric mucosa. Aldioxa was approved in Japan to improve subjective symptoms or objective of gastric/duodenal ulcer and gastritis. It was discovered, that aldioxa ameliorates delayed gastric emptying through its antagonistic activity on the α-2 adrenergic receptor. The most commonly reported adverse reactions include constipation.

Idazoxan is an alpha2 receptor antagonist which also shows activity at imidazoline I1 and I2 receptors and modulates the release of dopamine. Idazoxan was in phase II development in the US. Later the development of idazoxan for schizophrenia was discontinued. It was also in clinical trials for cognition disorders in United Kingdom, and was also discontinued. Idazoxan is used in scientific research as a tool for the study of alpha 2-adrenoceptors.

Fipamezole is a fluorine substituted imidazole compound with high antagonist specificity for the presynaptic alpha2-adrenoceptor. There were no significant differences between the affinity of Fipamezole for the different subtypes, thus characterizing Fipamezole as a non-subtype–selective alpha2 antagonist. Fipamezole had been in phase III clinical trials for the treatment of dyskinesia associated with Parkinson’s disease. Detected side effects are hypertension, nausea, vomiting, dysgeusia, facial flushing.

Dexefaroxan is a selective alpha 2-adrenergic receptor antagonist. Вexefaroxan improved TgCRND8 (protein-transgenic mouse model of Alzheimer's disease) behavioral phenotypes and increased BDNF mRNA expression without affecting amyloid-β peptide levels. Dexefaroxan treatment also enhanced the number and complexity of the dendritic arborizations of polysialated neural cell adhesion molecule-positive neurons. The trophic effects of dexefaroxan on newborn cells might involve an increase in brain-derived neurotrophic factor, which was upregulated in afferent noradrenergic fiber projection areas and in neurons in the granule cell layer. By promoting the survival of new endogenously formed neurons, dexefaroxan treatment represents a potential therapeutic strategy for maintaining adult neurogenesis in neurodegenerative conditions, such as Alzheimer's disease, that affect the hippocampus. Dexefaroxan increases neuron survival in the olfactory bulb of the adult rat in vivo, putatively as a result of reducing the apoptotic fate of telencephalic stem cell progenies.

Conessine is a plant steroid alkaloid that acts as a potent and specific antagonist of histamine H3 receptors. Conessine displayed high affinity at both rat and human H3 receptors (pKi = 7.61 and 8.27) and generally high selectivity against other sites, including histamine receptors H1, H2, and H4. Conessine was found to efficiently penetrate the CNS and reach very high brain concentrations. Although the very slow CNS clearance and strong binding to adrenergic receptors discouraged focus on conessine itself for further development, its potency and novel steroid-based skeleton motivated further chemical investigation. Modification based on introducing diversity at the 3-nitrogen position generated a new series of H3 antagonists with higher in vitro potency, improved target selectivity, and more favorable drug-like properties. Conessine also has high affinity for the adrenergic receptors. Conessine has being shown to possess anti-malarial activity. In India conessine finds therapeutic use for treatment of dysentery and helminthic disorders.

ICI-118,551 is a selective subtype β2 adrenergic receptor (adrenoreceptor) antagonist. ICI-118,551 binds to the β2 subtype with at least 100 times greater affinity than to other subtypes of the beta adrenoceptor β1 or β3. Pharmacological experiments proved that the right shift of the norepinephrine dose-response curve by ICI-118,551 was mediated via a beta(2)-adrenoceptor/G(i/o) protein-dependent pathway enhancing NO production in the endothelium. These results were corroborated in beta-adrenoceptor and endothelial NO synthase knockout mice where ICI had no effect. ICI-118,551 increased vascular lumen diameter in lung sections and reduced pulmonary arterial pressure under normoxia and under hypoxia in the isolated perfused lung model. These effects were found to be physiologically relevant, because ICI-118,551 specifically decreased pulmonary but not systemic blood pressure in vivo. Thus, it has been suggested that ICI-118,551 is a pulmonary arterial-specific vasorelaxant and might be a potential novel therapeutic agent for the treatment of pulmonary arterial hypertension. It was also demonstrated that systemic topical administration of ICI 118,551 results in decreased intraocular pressure in both eyes of rabbits, indicating that at least part of the ocular hypotensive effect of topical ICI 118,551 is mediated through systemic absorption. However, ICI 118,551 did not lower blood pressure in hypertensive patients known to respond to therapy with atenolol or propranolol.

(+)-octopamine is an enantiomer of octopamine, a naturally occurring phenolamine acting as a neurotransmitter in invertebrates. Octopamine is considered to be trace amine present in mammalian tissues at very low (nanomolar) concentrations. Generally, the (+)-enantiomers of octopamine are less active than the (-)-enantiomers at adrenergic receptors. However (+)-octopamine is more potent than the (-)-octopamine as an inhibitor of semicarbazide-sensitive amine oxidase.

(-)-octopamine is an enantiomer of octopamine, a naturally occurring phenolamine acting as a neurotransmitter in invertebrates. Octopamine is considered to be trace amine present in mammalian tissues at very low (nanomolar) concentrations. Generally, the (-)-enantiomers of octopamine are more active than the (+)-enantiomers at adrenergic receptors. However (+)-octopamine is more potent than the (-)-octopamine as an inhibitor of semicarbazide-sensitive amine oxidase.

BRL-44408, a potent (Ki=8.5 nM) and selective (>50-fold) α2A-adrenoceptor antagonist (KB=7.9 nM). BRL-44408 revealed antidepressant- and analgesic-like activity through selective alpha2A-adrenoceptor antagonism. Preclinical characterization of the neurochemical and behavioural profile of BRL-44408 suggests that selective antagonism of alpha2A-adrenoceptors may represent an effective treatment strategy for mood disorders and visceral pain. BRL-44408 increases hippocampal noradrenalin release following systemic administration. BRL-44408 has potential therapeutic application in the treatment of extrapyramidal side effects produced by some antipsychotic medications.