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Study Evaluating the Long-Term Safety of Desvenlafaxine Succinate Sustained-Release (DVS SR) in Subjects With Pain Associated With Diabetic Peripheral Neuropathy

2014-07-24 14:10:18 | BioPortfolio

Summary

The purpose of the study is to learn if long-term treatment with DVS SR is safe for treating the pain and other symptoms associated with diabetic peripheral neuropathy.

Study Design

Allocation: Non-Randomized, Endpoint Classification: Safety Study, Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Treatment

Conditions

Diabetic Neuropathy, Painful

Intervention

Desvenlafaxine Succinate Sustained-Release (DVS SR)

Status

Terminated

Source

Wyeth

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-07-24T14:10:18-0400

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Medical and Biotech [MESH] Definitions

Peripheral, autonomic, and cranial nerve disorders that are associated with DIABETES MELLITUS. These conditions usually result from diabetic microvascular injury involving small blood vessels that supply nerves (VASA NERVORUM). Relatively common conditions which may be associated with diabetic neuropathy include third nerve palsy (see OCULOMOTOR NERVE DISEASES); MONONEUROPATHY; mononeuropathy multiplex; diabetic amyotrophy; a painful POLYNEUROPATHY; autonomic neuropathy; and thoracoabdominal neuropathy. (From Adams et al., Principles of Neurology, 6th ed, p1325)

A cyclohexanol and phenol derivative and metabolite of venlafaxine that functions as a SEROTONIN AND NORADRENALINE REUPTAKE INHIBITOR (SNRI) and is used as an ANTIDEPRESSIVE AGENT.

Enzymes that catalyze the first step leading to the oxidation of succinic acid by the reversible formation of succinyl-CoA from succinate and CoA with the concomitant cleavage of ATP to ADP (EC 6.2.1.5) or GTP to GDP (EC 6.2.1.4) and orthophosphate. Itaconate can act instead of succinate and ITP instead of GTP.EC 6.2.1.-.

Glycogenosis due to muscle phosphorylase deficiency. Characterized by painful cramps following sustained exercise.

An enzyme that plays a role in the GLUTAMATE and butanoate metabolism pathways by catalyzing the oxidation of succinate semialdehyde to SUCCINATE using NAD+ as a coenzyme. Deficiency of this enzyme, causes 4-hydroxybutyricaciduria, a rare inborn error in the metabolism of the neurotransmitter 4-aminobutyric acid (GABA).

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