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Details

Stereochemistry MIXED
Molecular Formula C17H24O3
Molecular Weight 276.3707
Optical Activity UNSPECIFIED
Defined Stereocenters 0 / 3
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of CYCLANDELATE

SMILES

CC1CC(CC(C)(C)C1)OC(=O)C(O)C2=CC=CC=C2

InChI

InChIKey=WZHCOOQXZCIUNC-UHFFFAOYSA-N
InChI=1S/C17H24O3/c1-12-9-14(11-17(2,3)10-12)20-16(19)15(18)13-7-5-4-6-8-13/h4-8,12,14-15,18H,9-11H2,1-3H3

HIDE SMILES / InChI

Description

Cyclandelate is a vasodilator developed for the treatment of cardiovascular diseases. The drug was used in many countries for such diseases as intermittent claudication, arteriosclerosis obliterans, thrombophlebitis, nocturnal leg cramps, local frostbite, Raynaud's phenomenon. In the USA it was also approved for intermittent claudication and cognitive dysfunction in Alzheimer's disease under the name Cyclospasmol. Cyclandelate exerts its effect by blocking calcium channels and inhibiting smooth muscles contration. Cyclandelate was withdrawn from the market in the USA for lack of effectiveness.

CNS Activity

Originator

Approval Year

Targets

Primary TargetPharmacologyConditionPotency

Conditions

ConditionModalityTargetsHighest PhaseProduct
Primary
CYCLOSPASMOL
Palliative
CYCLOSPASMOL

Doses

PubMed

Sample Use Guides

In Vivo Use Guide
The usual dose of cyclandelaye is between 400 - 800 mg per day, given in two or four divided doses. If indicated, higher doses of 1200 mg to 1600 mg per day may be given in four divided doses before meals and at bedtime, for two to four weeks, and then reduced by 200 mg decrements to the usual dose.
Route of Administration: Oral
In Vitro Use Guide
Cyclandelate in concentrations between 10 and 50 uM induced a dose-dependent increase in the basal level of cytosolic Ca++ of unstimulated platelets. In platelets stimulated with thrombin (5 U/ml) or platelet activating factor (1 uM), cyclandelate strongly inhibited the increase of cystolic Ca++ in the presence of extracellular Ca++, but in the absence of extracellular Ca++ only a weak inhibition was observed. This inhibition was dose dependent and optimal at about 50 uM, the concentration at which Ca++ mobilisation was suppressed to about 10% of control values, and at which cyclandelate inhibits platelet aggregation.