Grant: Project Grant
University of Ottawa
$673,200.00
Novel therapy for Hyperkalemic Periodic Paralysis (HyperKPP)
EF 2016-17
Résumé
Hyperkalemic Periodic Paralysis (HyperKPP) is a neuromuscular disease that is characterized by periods of myotonia weakness and paralysis. Few treatment options are available to patients suffering of HyperKPP, and in many cases they lose efficacy over time. Using a HyperKPP mouse model, we first found that HyperKPP muscles are weaker than normal; i.e., they generate less force. Then, we found that activating two proteins in the cell membrane, an ion transporter and one ion channel, can provide a novel therapy that fully restores force development back to normal levels. There is also evidence that the activity of two of these proteins can be increased using a drug that activates protein kinase A (PKA). This is advantageous because a single drug can be used to activate PKA instead of two drugs, reducing the extent of side effects. More importantly, it is proposed to test the efficacy of three already Federal Drug Administration (FDA) approved drugs that are used to treat various diseases via an activation of protein kinase A. In a first series of experiments, we will determine in vitro how effective each of three drugs is at increasing force generation in HyperKPP muscles toward that of normal muscles. In a second series of experiments, we will treat HyperKPP mice with the most effective drug to determine how effective they are at improving force generation over long period of time; i.e., to make sure they do not lose effectiveness over time. If successful, the ultimate aim will be to initiate clinical trials.
Programme
Project Grant
Bénéficiaire
Emplacement
Ontario, Canada
Type de bénéficiaire
Academia
Type
Grant
Source
CIHR Funding Decisions Database
Tel que publié
Id
355024
Name
Renaud Jean-Marc E
Region
Ontario
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Musculoskeletal Health and Arthritis
Theme2
Biomedical
Prcname2
Project Grant Competition
Projecttitle
Novel therapy for Hyperkalemic Periodic Paralysis (HyperKPP)
Programtype2
Operating Grants
Orgnameinp2
University of Ottawa
Cihramount2
$673,200
Cihrequipment2
$0
Programname2
Project Grant
Keyworddelim
Adenylate Cyclase; Channelopathy; Clc-1 Cl Channel; Hyperkalemic Periodic Paralysis; Katp Channel; Phosphodiesterase; Pka; Pkc; Skeletal Muscle; Sodium Potassium Atpase Pump
Abstract
Hyperkalemic Periodic Paralysis (HyperKPP) is a neuromuscular disease that is characterized by periods of myotonia weakness and paralysis. Few treatment options are available to patients suffering of HyperKPP, and in many cases they lose efficacy over time. Using a HyperKPP mouse model, we first found that HyperKPP muscles are weaker than normal; i.e., they generate less force. Then, we found that activating two proteins in the cell membrane, an ion transporter and one ion channel, can provide a novel therapy that fully restores force development back to normal levels. There is also evidence that the activity of two of these proteins can be increased using a drug that activates protein kinase A (PKA). This is advantageous because a single drug can be used to activate PKA instead of two drugs, reducing the extent of side effects. More importantly, it is proposed to test the efficacy of three already Federal Drug Administration (FDA) approved drugs that are used to treat various diseases via an activation of protein kinase A. In a first series of experiments, we will determine in vitro how effective each of three drugs is at increasing force generation in HyperKPP muscles toward that of normal muscles. In a second series of experiments, we will treat HyperKPP mice with the most effective drug to determine how effective they are at improving force generation over long period of time; i.e., to make sure they do not lose effectiveness over time. If successful, the ultimate aim will be to initiate clinical trials.
Competitiondate
201610
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Renaud, Jean-Marc E
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $673,200~ $0~