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Status:
Other
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Pseudopelletierine is the main alkaloid derived from the root-bark of the pomegranate tree (Punica granatum). Pseudopelletierine is used as an enzyme substrate.
Status:
Other
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Pseudopelletierine is the main alkaloid derived from the root-bark of the pomegranate tree (Punica granatum). Pseudopelletierine is used as an enzyme substrate.
Status:
Other
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Lycorine is a natural pyrrolo[de]phenanthridine ring-type alkaloid extracted from Amaryllidaceae. It has been reported to exhibit a wide range of physiological effects, including anti-viral, anti-malarial, anti-cancer and anti-inflammatory. Although a defined target or mechanism of action of lycorine is still unknown, it is a candidate anti-inflammatory and anti-cancer drug.
Status:
Other
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Lycorine is a natural pyrrolo[de]phenanthridine ring-type alkaloid extracted from Amaryllidaceae. It has been reported to exhibit a wide range of physiological effects, including anti-viral, anti-malarial, anti-cancer and anti-inflammatory. Although a defined target or mechanism of action of lycorine is still unknown, it is a candidate anti-inflammatory and anti-cancer drug.
Status:
Other
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
SB-271046 is one of the first selective 5-HT6 receptor antagonists to be discovered. SB-271046 is a
potent, selective and orally active 5-HT6 receptor antagonist with a pKi value of 8.9. This compound provides a useful tool for further elucidating
the physiological function of 5-HT6 receptors in vivo. SB-271046 was found to increase levels of the excitatory amino acid neurotransmitters glutamate and aspartate, as well as dopamine and noradrenaline in the frontal cortex and hippocampus of rats, and 5-HT6 antagonists have been shown to produce nootropic effects in a variety of animal studies. Suggested applications of SB-271046 included treatment of schizophrenia and other psychiatric disorders. A phase I clinical development of SB-271046 by GlaxoSmithKline (GSK) was discontinued due to a poor BBB permeability.
Status:
Other
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
FK-960 [N-(4-acetyl-1-piperazinyl)-p-fluorobenzamide monohydrate], a novel putative anti-dementia drug of piperazine derivative, ameliorates memory deficits in a variety of animal models of dementia in rats and monkeys, and also augments long-term potentiation (LTP) in the mossy fiber-CA3 pathway in guinea-pig hippocampal slices. FK-960 acts as Serotonin modulator. FK-960 had been in phase II clinical trials by Fujisawa Pharmaceutical (now Astellas) for the treatment of Alzheimer's disease (AD). However this study was suspended. In 2003 Phase-II for Alzheimer's disease in USA was discontinued and in Jul 2004 - Phase-II for Cognition disorders in Europe.
Status:
Other
Class (Stereo):
CHEMICAL (ABSOLUTE)
PHA-543613 was discovered by Pfizer and has been under development primarily as a potential treatment of schizophrenia. PHA-543613 acts as an agonist to the Neuronal acetylcholine receptor protein alpha-7 subunit. A single human trial was conducted in healthy human volunteers, but the compound has been studied extensively in rat models for schizophrenia as well as Parkinson's disease and Alzheimer's disease.
Status:
US Previously Marketed
Source:
COGNEX by SHIONOGI INC
(1993)
Source URL:
First approved in 1993
Source:
COGNEX by SHIONOGI INC
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Tacrine is a parasympathomimetic- a reversible cholinesterase inhibitor that is indicated for the treatment of mild to moderate dementia of the Alzheimer's type. An early pathophysiological feature of Alzheimer's disease that is associated with memory loss and cognitive deficits is a deficiency of acetylcholine as a result of selective loss of cholinergic neurons in the cerebral cortex, nucleus basalis, and hippocampus. Tacrine is postulated to exert its therapeutic effect by enhancing cholinergic function. This is accomplished by increasing the concentration of acetylcholine at cholinergic synapses through reversible inhibition of its hydrolysis by acetylcholinesterase. If this proposed mechanism of action is correct, tacrine's effect may lessen as the disease progresses and fewer cholinergic neurons remain functionally intact. There is no evidence that tacrine alters the course of the underlying dementing process. The mechanism of tacrine is not fully known, but it is suggested that the drug is an anticholinesterase agent which reversibly binds with and inactivates cholinesterases. This inhibits the hydrolysis of acetylcholine released from functioning cholinergic neurons, thus leading to an accumulation of acetylcholine at cholinergic synapses. The result is a prolonged effect of acetylcholine. is used for the palliative treatment of mild to moderate dementia of the Alzheimer's type. Tacrine was marketed under the trade name Cognex. Because of its liver toxicity and attendant requirement for monitoring liver function, tacrine prescriptions dropped after other acetylcholinesterase inhibitors were introduced, and its use has been largely discontinued.
Status:
US Previously Marketed
Source:
COGNEX by SHIONOGI INC
(1993)
Source URL:
First approved in 1993
Source:
COGNEX by SHIONOGI INC
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Tacrine is a parasympathomimetic- a reversible cholinesterase inhibitor that is indicated for the treatment of mild to moderate dementia of the Alzheimer's type. An early pathophysiological feature of Alzheimer's disease that is associated with memory loss and cognitive deficits is a deficiency of acetylcholine as a result of selective loss of cholinergic neurons in the cerebral cortex, nucleus basalis, and hippocampus. Tacrine is postulated to exert its therapeutic effect by enhancing cholinergic function. This is accomplished by increasing the concentration of acetylcholine at cholinergic synapses through reversible inhibition of its hydrolysis by acetylcholinesterase. If this proposed mechanism of action is correct, tacrine's effect may lessen as the disease progresses and fewer cholinergic neurons remain functionally intact. There is no evidence that tacrine alters the course of the underlying dementing process. The mechanism of tacrine is not fully known, but it is suggested that the drug is an anticholinesterase agent which reversibly binds with and inactivates cholinesterases. This inhibits the hydrolysis of acetylcholine released from functioning cholinergic neurons, thus leading to an accumulation of acetylcholine at cholinergic synapses. The result is a prolonged effect of acetylcholine. is used for the palliative treatment of mild to moderate dementia of the Alzheimer's type. Tacrine was marketed under the trade name Cognex. Because of its liver toxicity and attendant requirement for monitoring liver function, tacrine prescriptions dropped after other acetylcholinesterase inhibitors were introduced, and its use has been largely discontinued.
Status:
US Previously Marketed
Source:
Hydergine by Sandoz
(1951)
Source URL:
First approved in 1951
Source:
Hydergine by Sandoz
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Dihydroergocornine is an ergot alkaloid, one of the three components of ergoloid (trade name Hydergine). Dihydroergocornine (as the component of Ergoloid mesylates) has been used to treat dementia and age-related cognitive impairment (such as in Alzheimer disease), as well as to aid in recovery after stroke. There is no specific evidence which clearly establishes the mechanism by which Hydergine® (ergoloid mesylates) preparations produce mental effects, nor is there conclusive evidence that the drug particularly affects cerebral arteriosclerosis or cerebrovascular insufficiency. Hydergine may stimulates dopaminergic and serotonergic receptors and blocks alpha-adrenoreceptors.