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Status:
Other
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
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.
Status:
Other
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
(+)-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.
Status:
Other
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
(-)-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.
Status:
Other
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
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. In the pithed rat, only (-)- idazoxan possesses both alpha-1 and alpha-2 agonistic effects.
Status:
Other
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
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.
Status:
US Previously Marketed
Source:
21 CFR 310.528(a) aphrodisiac yohimbinum
Source URL:
First approved in 2015
Source:
NADA140866
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Yohimbine is a plant alkaloid with alpha-2-adrenergic blocking activity. Yohimbine has been used as a mydriatic and in the treatment of impotence. The exact mechanism for its use in impotence has not been fully elucidated. Yohimbine exerts antagonist actions at halpha(2A)-AR, h5-HT(1B), h5-HT(1D), and hD(2) sites, partial agonist actions at h5-HT(1A) sites. Yohimbine-mediated norepinephrine release at the level of the corporeal tissues may also be involved. In addition, beneficial effects may involve other neurotransmitters such as dopamine and serotonin and cholinergic receptors. Yohimbine has a mild anti-diuretic action, probably via stimulation of hypothalmic center and release of posterior pituitary hormone. Reportedly yohimbine exerts no significant influence on cardiac stimulation and other effects mediated by (beta)-adrenergic receptors. Its effect on blood pressure, if any, would be to lower it; however, no adequate studies are at hand to quantitate this effect in terms of Yohimbine dosage. Side effect of Yohimbine include anxiety, tremor, palpitations, diarrhea, and supine hypertension.
Status:
US Previously Marketed
Source:
WYTENSIN by WYETH AYERST
(1982)
Source URL:
First approved in 1982
Source:
WYTENSIN by WYETH AYERST
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Guanabenz, an antihypertensive agent for oral administration-, is an aminoguanidine derivative, 2,'6-dichlorobenzylideneamina-guanidine acetate. It is white to an almost white powder having not more than a slight odor. Sparingly soluble in water and in 0.1 N hydrochloric acid; soluble in alcohol and in propylene glycol.
Guanabenz is an orally active central alpha-2 adrenergic agonist. Its antihypertensive action appears to be mediated via stimulation of central alpha-adrenergic receptors, resulting in a decrease of sympathetic outflow from the brain at the bulbar level to the peripheral circulatory system. In clinical trials, guanabenz acetate, given orally to hypertensive patients, effectively controlled blood pressure without any significant effect on glomerular filtration rate, renal blood flow, body fluid volume or body weight. The Myelin Repair Foundation and the National Institutes of Health (National Institute of Neurological Disorders and Stroke) are developing guanabenz for the treatment of multiple sclerosis. Unlike the currently available treatment for multiple sclerosis that suppresses the immune system, guanabenz, an FDA approved the drug for the treatment of high blood pressure, has a potential to reduce the loss of myelin by protecting and repairing myelin-producing cells in the brain from damage. Phase I development is underway in the US.
Status:
US Previously Marketed
Source:
HYLOREL by PHARMACIA AND UPJOHN
(1982)
Source URL:
First approved in 1982
Source:
HYLOREL by PHARMACIA AND UPJOHN
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Conditions:
Guanadrel is a postganglionic adrenergic blocking agent. Uptake of guanadrel and storage in sympathetic neurons occurs via the norepinephrine pump or transporter. Guanadrel slowly displaces norepinephrine from its storage in nerve endings and thereby blocks the release of norepinephrine normally produced by nerve stimulation. The reduction in neurotransmitter release in response to sympathetic nerve stimulation, as a result of catecholamine depletion, leads to reduced arteriolar vasoconstriction, especially the reflex increase in sympathetic tone that occurs with a change in position. Guanadrel is used to treat and control hypertension.
Status:
US Previously Marketed
First approved in 1952
Source:
RAVOCAINE AND NOVOCAIN W/ NEO-COBEFRIN by EASTMAN KODAK
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Levonordefrin acts as a topical nasal decongestant and vasoconstrictor, most often used in dentistry. It is administered in a pre-mixed solution with local anesthetics, such as mepivacaine or procaine.