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Search results for guanidine in Any Name (approximate match)
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
Source:
TENATHAN by ROBINS AH
(1981)
Source URL:
First approved in 1981
Source:
TENATHAN by ROBINS AH
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Bethanidine is a post-ganglionic adrenergic neurone-blocking agent which exerts a marked postural hypotensive effect. The precise mechanism whereby bethanidine causes blockade of adrenergic neurones is unknown. An initial sympathomimetic effect has been demonstrated in man and animals, possibly due to release of catecholamines.
Status:
US Previously Marketed
Source:
GUANETHIDINE MONOSULFATE by WATSON LABS
(1985)
Source URL:
First approved in 1960
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Guanethidine belongs to the general class of medicines called antihypertensives. It was used to treat high blood pressure (hypertension). It is believed to act mainly by preventing the release of norepinephrine at nerve endings and causes depletion of norepinephrine in peripheral sympathetic nerve terminals as well as in tissues. It is taken up by norepinephrine transporters. It becomes concentrated in NE transmitter vesicles, replacing NE in these vesicles.
Status:
US Previously Marketed
Source:
Pre-Creatine glycocyamine by Mercury Pharmaceuticals
(1958)
Source URL:
First approved in 1958
Source:
Pre-Creatine glycocyamine by Mercury Pharmaceuticals
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
US Previously Marketed
Source:
GUANIDINE HYDROCHLORIDE by MERCK SHARP DOHME
(1939)
Source URL:
First approved in 1939
Source:
GUANIDINE HYDROCHLORIDE by MERCK SHARP DOHME
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Guanidine is a small basic compound. Guanidine stimulates the neuromuscular junction presynaptically by inhibiting voltage-gated potassium (Kv) channels, leading to the enhanced release of acetylcholine in the synaptic cleft. This stimulatory effect of guanidine underlies its use in the therapy for the neuromuscular diseases. The hydrochloride salt of guanidine was approved by FDA for the reduction of the symptoms of muscle weakness and easy fatigability associated with the myasthenic syndrome of Eaton-Lambert.
Status:
Possibly Marketed Outside US
Source:
21 CFR 352
(2015)
Source URL:
First approved in 2015
Source:
21 CFR 352
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Possibly Marketed Outside US
Source:
21 CFR 352
(2010)
Source URL:
First approved in 2010
Source:
21 CFR 352
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Biguanide has been investigated for the treatment of Diabetes Mellitus. The term "biguanidine" often refers specifically to a class of drugs that have a broad range of medical indications. Besides recent experiments have shown that biguanide could be a modifiable pharmacophore for the synthesis of therapeutic cysteinyl cathepsins inhibitors with a wide range of potencies and specificities. It is known that excessive activities of cysteinyl cathepsins contribute to the progress of many diseases.
Status:
Possibly Marketed Outside US
Source:
Arpromidine by Onbio Inc.
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Arpromidine is a potent histamine H2-receptor agonist and weak NPY Y1 antagonist. In the isolated aperfused heart, arpromidine was more potent in increasing cardiac contractile force and coronary flow but less effective on heart rate and less arrhythmogenic. Arpromidine may be considered a new lead for the development of "cardiohistaminergics". In the arpromidine series the order of potency found in guinea-pig atria was in good agreement with the results from isolated perfused guinea-pig hearts. In particular, the two-fold halogenated arpromidine analogues proved to be more potent positive inotropic agents than impromidine with lower stimulating effects on heart rate and reduced arrhythmogenic properties.
Status:
Possibly Marketed Outside US
Source:
Japan:Adrenochrome Monoaminoguanidine Mesilate
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Conditions:
Adrenochrome monoaminoguanidine (S-Adchnon) is a hemostatic capillary-stabilizing agent demonstrating pharmacological effects against radiation injury by reducing side effects of radiation therapy on hematopoietic organ. Synthesized by a dehydrating reaction of adrenochrome and aminoguanidine it has superior properties than adrenochrome, an oxidation product of adrenalin remarkable for its efficiency as a haemostatic agent at very small doses and for its more rapid and equally intense action than that of adrenalin. Adrenochrome does not alter the cardiac rhythm and does not cause any hypertension or internal haemorrhages and would be suitable for therapeutic applications, however, its instability, in aqueous or alcoholic solution, makes its use substantially impossible. S-Adchnon was devised, approved by the Japanese Ministry of Health, Labor and Welfare in 1962 and used widely in Japan. Adrenochrome monoaminoguanidine has negligible toxicity, stable and could be made into salts for aqueous dosage, especially for injection. Adrenochrome monoaminoguanidine methanesulfonate (AMM) enhances the recovery from radiation-induced leukopenia in rabbits and in humans, and inhibits the increases in chromosome aberrations in peripheral lymphocytes of patients with cervical carcinoma under radiotherapy. It has been shown that the radiation-induced initial decrease in number of peripheral blood leukocytes (PBL) is not affected by AMM, but recovery from the decrease is enhanced, shortening the period of leukopenia. This suggests that AMM may not exert its effects by protecting PBL directly but by protecting stem and/or progenitor cells in hematogenesis which proliferate and differentiate to PBL after irradiation. In in vitro colony formation method AMM demonstrated a protective effect on the survival of GM-CFC, a hematopoietic progenitor cells. Differential action on cancer and normal tissue by AMM and cytochrome C combined with radiotherapy was demonstrated. AMM in combination with cytochrome C augumented natural killer (NK) cells activity in KSN nude mice, protected potent NK cells in patients with lung cancer against radiotherapy and sensitized the human lung cancer xenografts to radiotherapy. Thus, AMM and cytochrome C may have the potential as a differential modulator of radiosensitivity of normal tissues and of tumors.