Abstract: The invention relates to improved alkaline phosphatases, pharmaceutical compositions comprising improved alkaline phosphatases and the use of improved alkaline phosphatases for preventing, treating or curing diseases.

Abstract: Methods are disclosed for treating periodontal disease, peri-implantitis, or to preserve a tooth socket in a subject. These methods include selecting a subject with periodontal disease, peri-implantitis, or in need of tooth socket preservation; and locally administering into the periodontium of the subject a therapeutically effective amount of a tissue-nonspecific alkaline phosphatase (TNAP) polypeptide, or a nucleic acid molecule encoding the recombinant TNAP polypeptide. Methods are also disclosed for i) promoting alveolar bone regeneration in the subject; ii) increasing attachment of a periodontal ligament to a root surface of a tooth in the subject; iii) increasing cementum formation; and/or iv) increasing mineralization in a tooth in the subject. Pharmaceutical compositions are also disclosed that are of use in these methods.

Abstract: Described herein are methods of treating atherosclerosis, including administering a tissue-nonspecific alkaline phosphatase (TNAP) inhibitor to a patient. Described herein are also methods of reducing microcalcifications in an atherosclerotic plaque, including administering a TNAP inhibitor to a patient. Described herein are also methods of preventing, arresting, or reducing the development of plaque calcifications in a patient, including administering a TNAP inhibitor to a patient.

Abstract: The invention relates to improved alkaline phosphatases, pharmaceutical compositions comprising improved alkaline phosphatases and the use of improved alkaline phosphatases for preventing, treating or curing diseases.

Abstract: The invention relates to improved alkaline phosphatases, pharmaceutical compositions comprising improved alkaline phosphatases and the use of improved alkaline phosphatases for preventing, treating or curing diseases.

Abstract: Described herein are compounds that modulate the activity of TNAP. In some embodiments, the compounds described herein inhibit TNAP. In certain embodiments, the compounds described herein are useful in the treatment of conditions associated with hyper-mineralization.

Abstract: The invention relates to improved alkaline phosphatases, pharmaceutical compositions comprising improved alkaline phosphatases and the use of improved alkaline phosphatases for preventing, treating or curing diseases.

Abstract: Described herein are compounds that modulate the activity of TNAP. In some embodiments, the compounds described herein inhibit TNAP. In certain embodiments, the compounds described herein are useful in the treatment of conditions associated with hyper-mineralization.

Abstract: The invention relates to improved alkaline phosphatases, pharmaceutical compositions comprising improved alkaline phosphatases and the use of improved alkaline phosphatases for preventing, treating or curing diseases.

Abstract: Described herein are compounds that modulate the activity of TNAP. In some embodiments, the compounds described herein inhibit TNAP. In certain embodiments, the compounds described herein are useful in the treatment of conditions associated with hyper-mineralization.

Abstract: The invention relates to improved alkaline phosphatases, pharmaceutical compositions comprising improved alkaline phosphatases and the use of improved alkaline phosphatases for preventing, treating or curing diseases.

Abstract: Described herein are compounds that modulate the activity of TNAP. In some embodiments, the compounds described herein inhibit TNAP. In certain embodiments, the compounds described herein are useful in the treatment of conditions associated with hyper-mineralization.

Abstract: Described herein are compounds that modulate the activity of TNAP. In some embodiments, the compounds described herein inhibit TNAP. In certain embodiments, the compounds described herein are useful in the treatment of conditions associated with hyper-mineralization.

Abstract: Described herein are compounds that modulate the activity of TNAP. In some embodiments, the compounds described herein inhibit TNAP. In certain embodiments, the compounds described herein are useful in the treatment of conditions associated with hyper-mineralization.

Abstract: Disclosed herein are compounds that are tissue-nonspecific alkaline phosphatase inhibitors. The disclosed compounds are used to treat, prevent, or abate vascular calcification, arterial calcification and other cardiovascular diseases.

Abstract: Disclosed herein are compounds that are tissue-nonspecific alkaline phosphatase inhibitors. The disclosed compounds are used to treat, prevent, or abate vascular calcification, arterial calcification and other cardiovascular diseases.

Abstract: This invention relates generally to the field of mineralization, and specifically to the role of TNAP in regulating the levels of extracellular inorganic pyrophosphate. The invention provides methods for modulating the activity of TNAP activity; methods for screening for modulators of TNAP activity; modulators of TNAP activity; and methods for treating pathologic conditions known of suspected to be affected by modulation of TNAP activity.

Abstract: Disclosed herein are compounds that are tissue-nonspecific alkaline phosphatase inhibitors. The disclosed compounds are used to treat, prevent, or abate vascular calcification, arterial calcification and other cardiovascular diseases.

Abstract: 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.

Abstract: Disclosed are modulators, i.e., activators and inhibitors, of Intestinal Alkaline Phosphatase (IAP). Also disclosed are methods for treating bacterial infections of the intestinal tract and methods for maintaining the health of the intestinal tract using IAP activators. Further disclosed are methods to assist in weight gain of emaciated patients and those having reduced or negligible fat absorption using IAP inhibitors.