Methods for improving the gastrointestinal tolerability of biguanide compounds and for treating metabolic disorders and/or inducing weight loss in patients in need thereof, particularly in individuals having a contraindication for treatment with biguanide compounds, are provided comprising administering delayed release formulations of such biguanide compounds, including metformin, targeted to the small intestine.

Methods for improving the gastrointestinal tolerability of biguanide compounds and for treating metabolic disorders and/or inducing weight loss in patients in need thereof, particularly in individuals having a contraindication for treatment with biguanide compounds, are provided comprising administering delayed release formulations of such biguanide compounds, including metformin, targeted to the small intestine.

Methods for improving the gastrointestinal tolerability of biguanide compounds and for treating metabolic disorders and/or inducing weight loss in patients in need thereof, particularly in individuals having a contraindication for treatment with biguanide compounds, are provided comprising administering delayed release formulations of such biguanide compounds, including metformin, targeted to the small intestine.

Embodiments of calcium channel agonists, as well as methods of making and using the calcium channel agonists, are disclosed. The disclosed calcium channel agonists and corresponding salt forms have a structure according to general formula I:

##STR00001##

wherein each bond depicted as “” is a single bond or a double bond as needed to satisfy valence requirements; Z.sup.1, Z.sup.2, Z.sup.3, Z.sup.4, and Z.sup.5 independently are nitrogen or carbon; R.sup.1 and R.sup.3 are alkyl; R.sup.2 is alkyl, aryl, heteroaryl, arylalkyl, or heteroarylalkyl; and R.sup.4 is alkyl or hydroxyalkyl.

Embodiments of calcium channel agonists, as well as methods of making and using the calcium channel agonists, are disclosed. The disclosed calcium channel agonists and corresponding salt forms have a structure according to general formula I:

##STR00001##

wherein each bond depicted as “” is a single bond or a double bond as needed to satisfy valence requirements; Z.sup.1, Z.sup.2, Z.sup.3, Z.sup.4, and Z.sup.5 independently are nitrogen or carbon; R.sup.1 and R.sup.3 are alkyl; R.sup.2 is alkyl, aryl, heteroaryl, arylalkyl, or heteroarylalkyl; and R.sup.4 is alkyl or hydroxyalkyl.

Embodiments of calcium channel agonists, as well as methods of making and using the calcium channel agonists, are disclosed. The disclosed calcium channel agonists and corresponding salt forms have a structure according to general formula I:

##STR00001##

wherein each bond depicted as “” is a single bond or a double bond as needed to satisfy valence requirements; Z.sup.1, Z.sup.2, Z.sup.3, Z.sup.4, and Z.sup.5 independently are nitrogen or carbon; R.sup.1 and R.sup.3 are alkyl; R.sup.2 is alkyl, aryl, heteroaryl, arylalkyl, or heteroarylalkyl; and R.sup.4 is alkyl or hydroxyalkyl.

This application relates to compounds of Formula I:

##STR00001##

or pharmaceutically acceptable salts thereof, which are inhibitors of TAM kinases which are useful for the treatment of disorders such as cancer.

This application relates to compounds of Formula I:

##STR00001##

or pharmaceutically acceptable salts thereof, which are inhibitors of TAM kinases which are useful for the treatment of disorders such as cancer.

Provided here are therapeutically effective pharmaceutical compositions containing one or more TREX2 inhibitors, and more specifically methods of administering TREX2 inhibitors to increase the effectiveness of a chemotherapeutic agent. Also provided here are methods of identifying agents that inhibit the exonuclease activity of TREX2.

Provided here are therapeutically effective pharmaceutical compositions containing one or more TREX2 inhibitors, and more specifically methods of administering TREX2 inhibitors to increase the effectiveness of a chemotherapeutic agent. Also provided here are methods of identifying agents that inhibit the exonuclease activity of TREX2.