Technologies

Pharmaceutical Sciences

Title:	CDRI Compound S007-1500 (Novel Orally Active Fracture Healing Drug Candidate)
Area:	Medical Sciences, Pharmaceutical Sciences
Focus Area:	Fracture Healing
Patent:	CN102264716, EP2346844, IN294021, JP5719775, KR101686607, US8686028
Social Benefits:	Potential osteogenic property and shows accelerated fracture repairing. New bone formation at the fracture site is increased by ~40% in rats, Increases callus formation at only 1 mg/kg dose and restores trabecular microarchitecture at fractured site in normal male and female and osteopenic rats, Increases bone healing in male and female New Zealand white rabbits at a dose as low as 1.0 mg.kg-1.day-1 , It leads to accelerated fracture repair by BMP-2/Smad signaling pathway, Compound found safe in single dose toxicity studies in rodents and in 10 days DRF studies, Essential Safety Pharmacology and Regulatory Toxicity study (Rodents and Non-rodents -dog) in GLP as per schedule Y/ FDA is completed and no mortality/adverse effect was observed, No orally active drug available in market. FDA has approved rhBMP-2 bone graft for open tibial fractures but it has several side effects and is very expensive, S007-1500 synthesis is industrially acceptable five step process. It will be cost effective and easily affordable, Will enable return to active life much faster
Developing Agency:	CSIR-Central Drug Research Institute (CDRI), Uttar Pradesh
Technology Readiness Index:	Technology Development
Email:	director@cdri.res.in
Website Link :	http://www.cdri.res.in
Source (more info) :	https://t.ly/l_sb

Brief Description

Description :

First-in-Class orally active fracture repairing drug candidate. Enhances osteoblast differentiation and mineralization at concentration as low as 1pM (EC50= 3.125 nM). Enhances new bone formation and restores bone microarchitecture in adult osteopenic rats. Enhances bone regeneration at fracture site at only 1 mg.kg-1.day-1 dose by stimulation of BMP/Smad signaling pathway . New bone formation at the fracture site is increased by ~40% in rats treated with S007-1500. S007-1500 enhances bone mineral density, new bone formation and bone biomechanical strength in ovariectomized osteopenic rat model. S007-1500 restores ovariectomized (Ovx) induced deterioration in bone microarchitecture. S007-1500 prevents Ovx induced increase in bone resorptive marker, CTx (a collagen breakdown product). S007-1500 prevents Ovx induced increase in bone turnover marker like serum OCN. Oral administration of S007-1500 at 1 mg/kg in rabbit critical size defect model led to almost complete bone healing at defect site as analyzed by radiography. S007-1500 is found safe in regulatory toxicity and safety pharmacology in GLP (rodents and non-rodents) as per Schedule “Y” and FDA guidelines.