The present disclosure generally relates to a process for manufacturing a microparticle composite or a dry powder inhaler composition of polymyxin and CFTR activator or CFTR potentiator comprising the steps preparing a suspension of nanoparticles (NPs) of CFTR activator or CFTR potentiator or their combinations; mixing the suspension of NPs with a solution of polymyxin and a solution of leucine, then followed by drying to afford said micro-particle composite or dry powder inhaler composition. Pharmaceutical compositions and methods for treating a patient of cystic fibrosis (CF) and/or a lung infection are within the scope of this invention.

The present disclosure generally relates to a process for manufacturing a microparticle composite or a dry powder inhaler composition of polymyxin and CFTR activator or CFTR potentiator comprising the steps preparing a suspension of nanoparticles (NPs) of CFTR activator or CFTR potentiator or their combinations; mixing the suspension of NPs with a solution of polymyxin and a solution of leucine, then followed by drying to afford said micro-particle composite or dry powder inhaler composition. Pharmaceutical compositions and methods for treating a patient of cystic fibrosis (CF) and/or a lung infection are within the scope of this invention.

The present invention discloses compounds of Formula (I), or pharmaceutically acceptable salts, esters, or prodrugs thereof: ##STR00001##
which inhibit Human Respiratory Syncytial Virus (HRSV) or Human Metapneumovirus (HMPV) inhibitors. The present invention further relates to pharmaceutical compositions comprising the aforementioned compounds for administration to a subject suffering from HRSV or HMPV infection. The invention also relates to methods of treating an HRSV or HMPV infection in a subject by administering a pharmaceutical composition comprising the compounds of the present invention.

This disclosure provides modulators of Cystic Fibrosis Transmembrane Conductance Regulator (CFTR), pharmaceutical compositions containing at least one such modulator, methods of treatment of cystic fibrosis using such modulators and pharmaceutical compositions, and processes for making such modulators.

This disclosure provides modulators of Cystic Fibrosis Transmembrane Conductance Regulator (CFTR), pharmaceutical compositions containing at least one such modulator, methods of treatment of cystic fibrosis using such modulators and pharmaceutical compositions, and processes for making such modulators.

The present invention relates to compounds of Formula I, pharmaceutically acceptable salts, solvates or formulations thereof. Compounds of Formula I increase significantly low density lipoprotein receptor and are useful for preventing and treating of elevated cholesterol.

The present invention provides oxaborole ester compounds and compositions thereof which are useful to treat diseases associated with parasites, such as Chagas Disease and African Animal Trypanosomosis.

The present invention provides oxaborole ester compounds and compositions thereof which are useful to treat diseases associated with parasites, such as Chagas Disease and African Animal Trypanosomosis.

A method of treating cancer or metastasis is provided involving administering at least one oncostatin M (OSM) antagonist to a subject, wherein the subject has been diagnosed with cancer. Administration of an OSM antagonist such as a small molecule pharmaceutical is provided as well as an anti-OSM antibody, an anti-OSM aptamer, and an OSM mRNA antagonist. The OSM antagonists were found to inhibit or prevent tumor cell detachment, progression, proliferation and metastasis in several cancer types.

The present invention provides, among other things, an improved method of treating cystic fibrosis (CF) in a human subject. The method comprises administration of a composition comprising an mRNA encoding a Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) protein by nebulization at a dose between 7 mg and 25 mg. A suitable dose for use in the method of the invention is selected on the basis that it provides the human subject with at least a 3% increase in absolute change in ppFEV1 (percent predicted forced expiratory volume in one second) from baseline ppFEV1 at two days following the administration. In addition or alternatively, the dose is selected to provide the human subject with at least a 2% increase in absolute change in ppFEV1 from baseline ppFEV1 at one week following the administration. In addition or alternatively, the dose is selected to provide the human subject with at least a 4% maximum increase in absolute change in ppFEV1 from baseline ppFEV1 through one week following administration.