ROBERT TERKELTAUB, M.D.
Osteopathic Medicine at Arbor Dr, San Diego, CA

2007002, Jan 25, 2007

Jun 29, 2005

11/172386

Robert Terkeltaub - San Diego CA, US
Anne Murphy - Encinitas CA, US
James Dykens - Encinitas CA, US
Soumitra Ghosh - San Diego CA, US
Robert Davis - San Diego CA, US
Andrew Granston - San Diego CA, US

MIGENIX Corp. - San Diego CA
THE REGENTS OF THE UNIVERSITY OF CALIFORNIA - Oakland CA

A61K 31/365

514450000

The present invention relates to improved diagnostic methods for early detection of a risk for developing an arthritic disorder in humans, and screening assays for therapeutic agents useful in the treatment of arthritic disorders, by comparing the levels of one or more indicators of altered mitochondrial function. Indicators of altered mitochondrial function include enzymes such as mitochondrial enzymes and ATP biosynthesis factors. Other indicators of altered mitochondrial function include mitochondrial mass, mitochondrial number and mitochondrial DNA content, cellular responses to elevated intracellular calcium and to apoptogens, and free radical production. Methods of treating, and of stratifying, human patients as such methods relate to disclosed indicators of altered mitchondrial function are also provided.

7005274, Feb 28, 2006

Sep 14, 2000

09/661848

Robert Terkeltaub - San Diego CA, US
Anne N. Murphy - Encinitas CA, US
James A. Dykens - Encinitas CA, US
Soumitra S. Ghosh - San Diego CA, US
Robert E. Davis - San Diego CA, US

MIGENIX Corp. - San Diego CA
The Regents of the University of California - Oakland CA

C12Q 1/02

435 29, 435 32, 435375

The present invention relates to improved diagnostic methods for early detection of a risk for developing an arthritic disorder in humans, and screening assays for therapeutic agents useful in the treatment of arthritic disorders, by comparing the levels of one or more indicators of altered mitochondrial function. Indicators of altered mitochondrial function include enzymes such as mitochondrial enzymes and ATP biosynthesis factors. Other indicators of altered mitochondrial function include mitochondrial mass, mitochondrial number and mitochondrial DNA content, cellular responses to elevated intracellular calcium and to apoptogens, and free radical production. Methods of treating, and of stratifying, human patients as such methods relate to disclosed indicators of altered mitchondrial function are also provided.

2002018, Dec 5, 2002

Mar 22, 2002

10/104482

Jose Millan - San Diego CA, US
Robert Terkeltaub - San Diego CA, US

Burnham Institute

A61K048/00, A61K031/198, A61K039/395

514/044000, 424/146100, 514/565000

The key function of TNAP in bone is degradation of PPi to remove this mineralization inhibitor and provide free phosphate for apatite deposition. PC-1 is a direct antagonist of TNAP function. ANK antagonizes TNAP-dependent matrix calcification. Specifically, the activity of PC-1 inhibits initial MV apatite deposition, but ANK inhibits propagation of apatite outside the MVs. Furthermore, loss of function of the two distinct skeletal TNAP antagonists, PC-1 and ANK, ameliorates TNAP deficiency-associated osteomalacia in vivo. Conversely, the hyperossification associated with both PC-1 null mice and ANK-deficient (ank/ank) mice is ameliorated by deficiency of TNAP in vivo.

2004010, Jun 10, 2004

Sep 23, 2003

10/669540

Robert Terkeltaub - San Diego CA, US

A61K048/00

424/085200, 514/044000

Methods of inhibiting calcification in meniscal and articular cartilage of the joints are disclosed. The methods include blocking the activation and activity of transglutaminases tTGase and Factor XIIIa. Furthermore, disclosed are methods for identifying agents that affect TGase activity and/or matrix calcification.

7888372, Feb 15, 2011

Apr 28, 2003

10/426005

Jose Luis Millan - San Diego CA, US
Robert Terkeltaub - San Diego CA, US

National Institutes of Health (NIH) - Bethesda MD
The Regents of the University of California - Oakland CA

A01N 43/42, A01N 37/12

514310, 514565

The key function of TNAP in bone is degradation of PPi to remove this mineralization inhibitor and provide free phosphate for apatite deposition. PC-1 is a direct antagonist of TNAP function. ANK also antagonizes TNAP-dependent matrix calcification. Specifically, the activity of PC-1 inhibits initial MV apatite deposition, but ANK inhibits propagation of apatite outside the MVs. Furthermore, loss of function of the two distinct skeletal TNAP antagonists, PC-1 and ANK, ameliorates TNAP deficiency-associated osteomalacia in vivo. Conversely, the hyperossification associated with both PC-1 null mice and ANK-deficient (ank/ank) mice is ameliorated by deficiency of TNAP in vivo.