Ergocristine is an alkoloid originally isolated from Iberian ergot. In the rat, ergocristine acts as an alpha 2-adrenoceptors agonist, and an alpha 1-adrenoceptors antagonist. It is able to regulate glutamate uptake and dopamine release. Ergocristine is controlled as a list I chemical of because it is considered as a chemical precursor used in the illicit manufacture of lysergic acid diethylamide,

Pseudoyohimbine is an alkaloid isolated from roots of Rauwolfia canescens and in trace amount from Uncaria attenuata. Also, it was found in the leaves, stem and bark of Alstonia quaternata and in root bark of Cabucala striolata and Catharanthus trichophyllus. Pseudoyohimbine is inactive in the periphery as well as in the central nervous system as an antagonist of a1- or a2-adrenoceptors.

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. Idazoxan`s diastereoisomers possess different relative selectivity for alpha2- pre- and postsynaptic receptors: ( )-idazoxan was 7-8 times more potent than (-)-idazoxan in inhibiting p-[3H]aminoclonidine binding, and 40 times more active in antagonizing clonidine at presynaptic level, indicating a better selectivity for alpha2-presynaptic sites. The pre- and postsynaptic alpha2-adrenoceptors have a different affinity for the two enantiomers of idazoxan. Although the stereoisomers are closely related structurally, ( )-idazoxan possesses a stronger affinity for presynaptic sites. This stereoselectivity was less evident for postsynaptic sites. In rats and dogs, both enantiomers antagonized the sympathoinhibitory effects of clonidine. In rats, ( )- idazoxan was 4-7 times more potent than (-)- idazoxan and 3-8 times more than (-)- idazoxan in dogs. A same order of potency was observed against the sedative effects of clonidine and azepexole in chicks, ( )- idazoxan being 8 times more potent than (-)- idazoxan. Although ( )- idazoxan was more potent than (-) idazoxan, binding studies revealed (-)- idazoxan to be more selective than ( )- idazoxan at central sites. It is concluded that ( )- idazoxan antagonizes both alpha-1 and alpha-2 adrenoceptors and (-)- idazoxan is selective for alpha-2 adrenoceptors. ( )- idazoxan is equipotent for antagonizing postsynaptic alpha-I and alpha-2 adrenoceptors. It is also a potent alpha-2 antagonist at presynaptic and central sites and is 4-8 times more potent than (-)- idazoxan but less selective.

(-)-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.

(+)-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.

(S)-carvedilol, an enantiomer of the drug carvedilol, which is used in the treatment of mild to moderate congestive heart failure. (S)-carvedilol is an alpha- and beta-adrenergic receptor blocker. It was shown, that only (S)-carvedilol caused beta-blockade. It was suggested, that the weak clinical net effect of beta-blockade of (R, S)-carvedilol at rest could be one reason why this drug causes fewer side effects than other beta-blockers, such as a reduction of nocturnal melatonin release.

(R)-carvedilol, an enantiomer of the drug carvedilol, which is used in the treatment of mild to moderate congestive heart failure. (R)-carvedilol is an alpha adrenergic receptor blocker. It was shown, that (R)-carvedilol increased sympathetic tone, presumably as a physiological reaction to the decrease in blood pressure caused by alpha-blockade. The weak clinical net effect of beta-blockade of (R, S)-carvedilol at rest might be one reason why this drug causes fewer side effects than other beta-blockers, such as a reduction of nocturnal melatonin release.

Alfuzosin, a quinazoline derivative, acts as a selective and competitive antagonist of alpha 1-adrenoceptor-mediated contraction of prostatic, prostatic capsule, bladder base and proximal urethral smooth muscle, thereby reducing the tone of these structures. Consequently, urethral pressure and resistance, bladder outlet resistance, bladder instability and symptoms associated with benign prostatic hyperplasia are reduced. The two enantiomers (S and R) have the same pharmacological activity as the racemate. Ligand binding and functional studies demonstrate that the alpha1-antagonist properties of alfuzosin reside equally in its two enantiomers. Racemic alfuzosin is indicated for the symptomatic treatment of benign prostatic hyperplasia and adjunctive therapy in acute urinary retention.

Alfuzosin, a quinazoline derivative, acts as a selective and competitive antagonist of alpha 1-adrenoceptor-mediated contraction of prostatic, prostatic capsule, bladder base and proximal urethral smooth muscle, thereby reducing the tone of these structures. Consequently, urethral pressure and resistance, bladder outlet resistance, bladder instability and symptoms associated with benign prostatic hyperplasia are reduced. The two enantiomers (S and R) have the same pharmacological activity as the racemate. Ligand binding and functional studies demonstrate that the alpha1-antagonist properties of alfuzosin reside equally in its two enantiomers. Racemic alfuzosin is indicated for the symptomatic treatment of benign prostatic hyperplasia and adjunctive therapy in acute urinary retention.