Register or Sign in to Save this opportunity, or Send an Inquiry.
Therapeutic Drug for Alzheimer's Disease Targeted Beta-amyloid Aggregation/ Toxicity Blocker_Medifron_DBT
Korea Health Industry Development Institute (KHIDI) South Korea flag South Korea
Abstract ID:
Therapeutic drug for Alzheimer's disease targeted beta-amyloid aggregation/ toxicity blocker
Send an Inquiry
RE:
Participants
You

1. Summary

Alzheimer's disease (AD) is worldwide 4th causing death

Number of AD patient increase rapidly coming after elderly society

Most of dementia is AD (over 60%)

The causing agent for AD is believed beta-amyloid peptide

In the brain, beta-amyloid over produced and make plaque outside neuron

Beta-amyloid in plaque is very resistance to protease attack

Solubilized beta-amyloid can be transfer to BBB through LRP receptor and eventually degraded

DWP09031 showed aggregation inhibitor as well as toxicity blocking activity

Proof of concept done by transgenic animal model

2. Applications

Neurodegenerative disease caused by protein aggregation

Alzheimer's disease

3. Market Feasibility

Global AD market reach to 10B US$

In US, every year over 100B US$ spend AD care cost

Disease modification drug can be developed and it will expend market size

4. Technical Advantages

Drug candidate for aggregation/toxicity blocker

DWP09031 is to bind beta-amyloid peptide and block aggregation of beta-amyloid, therefore toxic form of oligomers of beta-amyloid could not be formed and soluble beta-amyloid might be transported outside the brain via LRP, scavenger receptor of brain.

Using hippocampus, DWP09031 can be restore LTP(long term potentiation) after beta-amyloid challenge

In animal model, the concentrations of beta-amyloid are lowered by 50% in the brain and recover the memory deficit induced by toxic beta-amyloid in the brain.

Human clinical trial study results showed that maximum dose (single dose 2,000mg) did not showed any sign of toxicity.

5. Technical Highlighted Summary

The concentration of beta-amyloid is lowered by 50% in the brain after treatment of DWP09031

Recover the memory deficit induced by toxic beta-amyloid in the brain.



Relatively high bio-availability in rodent and non rodent species

Good BBB penetration profile of DWP09031. Over 20% more compound detected in brain than plasma



Less drug drug interaction prediction. Seven isoforms of CYP enzyme cannot inhibited by DWP09031



GLP-compliant safety studies on rodent and non rodent including 4 weeks repeated dose toxicity, genotoxicity and safety pharmacology were done.

More importantly, in vitro hERG channel study showed low binding potential.

No moderate and significant safety issues occurred during safety and toxicity studies.

GO PREMIUM TO GET PATENT INFORMATION
Type of Business Relationship Sought
• We are actively seeking partner for global clinical trials. <br />• Out licensing deals for world exclusive sales right except Kore
FEATURED
Last Updated Oct 2017
Technology Type THERAPEUTIC
Phase of Development CLINICAL TRIALS
GOVERNMENT INSTITUTE

Opportunity Contact