A Phase I Clinical Trial to Evaluate the Effect of Renal Impairment on Pharmacokinetics of NOX-E36
This is a multi center, open label, parallel group, single administration, phase I trial, in subjects with mild, moderate or severe renal impairment and a control group with normal renal function.
|Study Design:||Allocation: Randomized
Endpoint Classification: Pharmacokinetics Study
Intervention Model: Parallel Assignment
Masking: Open Label
Primary Purpose: Treatment
|Official Title:||A Phase I, Open Label, Parallel Group, Multi-center Single Dose Trial to Evaluate the Effect of Renal Impairment on Pharmacokinetics of NOX-E36|
- Pharmacokinetics [ Designated as safety issue: No ]
|Study Start Date:||June 2011|
|Study Completion Date:||October 2012|
|Primary Completion Date:||October 2012 (Final data collection date for primary outcome measure)|
All subjects included in this study will receive the same dose of NOX E36.
All subjects included in this study will receive the same dose of NOX E36. In previous clinical trials, single intravenous doses of NOX E36 up to 2 mg/kg body weight and single subcutaneous doses of up to 0.5 mg/kg body weight appeared to be safe and well tolerated in healthy volunteers. Pharmacokinetic analyses have shown dose linearity
Current diabetes therapy does not stop progression of the disease and the development of diabetes mellitus (DM)-associated complications. A major concern in DM-patients is renal impairment due to nephropathy leading to a reduced glomerular filtration rate (GFR). It has been established that chronic (sub)clinical inflammation is crucial for the onset and progression of DM.
CCL2, also known as Monocyte chemoattractant protein 1 (MCP 1) is a chemokine from the cysteine-cysteine family, secreted by leukocytes or tissue cells. CCL2 promotes monocyte emigration from the bone marrow, activates monocytes and macrophages and directs their migration to sites of inflammation. Recent animal studies and clinical trials indicate a critical involvement of CCL2 in DM and diabetic nephropathy, suggesting that CCL2 may be a potential target for therapeutic intervention in DM. Finally, protein overload and oxidative challenge of the diseased kidney was suggested to stimulate CCL2 expression in renal tubuli, thereby accelerating the progression of diabetic nephropathy.
As NOX E36 is designed to specifically target human MCP-1/CCL2. This study is performed to evaluate the role of renal impairment for adequate dosing recommendations in the planned target population.
|Balatonfüred, Hungary, 8230|
|Moldova, Republic of|
|Innophar Mo S.R.L.|
|Chisinau, Moldova, Republic of|
|Principal Investigator:||Boris Sazu, MD||INNOPHAR MO s.R.L.|
|Principal Investigator:||Éva Péterfai||DRC|