Patent classifications
A61P7/10
FORMULATIONS OF 3-(6-(1-(2,2-DIFLUOROBENZO[D][1,3]DIOXOL-5-YL) CYCLOPROPANECARBOXAMIDO)-3-METHYLPYRIDIN-2-YL)BENZOIC ACID
A pharmaceutical composition comprising Compound 1, (3-(6-(1-(2,2-difluorobenzo[d][1,3]dioxol-5-yl) cyclopropanecarboxamido)-3-methylpyridin-2-yl)benzoic acid), and at least one excipient selected from: a filler, a disintegrant, a surfactant, a binder, and a lubricant, the composition being suitable for oral administration to a patient in need thereof to treat a CFTR mediated disease such as Cystic Fibrosis. Processes of preparing pharmaceutical compositions comprising Compound 1 are also disclosed.
NON-PATHOGENIC F18 E. COLI STRAIN AND USE THEREOF
There is provided an isolated E. coli strain deposited at the International Depositary Authority of Canada (IDAC) on Jun. 20, 2013 and attributed accession number 200613-01. There is also provided methods of using this strain for preventing edema disease or diarrhea caused by an F18 pathogenic E. coli infection in an animal.
Pyrimidone Compounds Used as Lp-PLA2 Inhibitors and Pharmaceutical Compositions Thereof
The present invention relates to pyrimidone compounds used as Lp-PLA.sub.2 inhibitors and pharmaceutical compositions thereof. The structure of the pyrimidone compounds is represented by general formula (I), wherein R.sub.1, R.sub.2, R.sub.3, X, Ar, Y and n are defined as in the specification and claims. The compounds of general formula (I) in the present invention, stereoisomers and pharmaceutically acceptable salts thereof can be used as Lp-PLA.sub.2 inhibitors for preventing, treating and/or ameliorating diseases associated with the activity of Lp-PLA.sub.2 enzyme.
##STR00001##
Human plasma kallikrein inhibitors
Disclosed are compounds of formula I: ##STR00001## as described herein, and pharmaceutically acceptable salts thereof. The compounds are inhibitors of plasma kallikrein. Also provided are pharmaceutical compositions comprising at least one such compound, and methods involving use of the compounds and compositions in the treatment and prevention of diseases and conditions characterized by unwanted plasma kallikrein activity.
PHARMACEUTICAL COMBINATION COMPRISING A BRAIN AMINOPEPTIDASE A INHIBITOR, A DIURETIC AND A BLOCKER OF THE SYSTEMIC RENIN-ANGIOTENSIN SYSTEM
The present invention relates to a pharmaceutical combination comprising (i) firibastat, (ii) a diuretic and (iii) a blocker of the systemic renin-angiotensin system selected from the group consisting of angiotensin I converting enzyme inhibitors (ACEIs) and angiotensin II receptor type 1 (AT1R) antagonists. Said composition is particularly useful for the treatment of hypertension and related diseases and conditions.
USE OF AN ANTI-FACTOR XII ANTIBODY FOR THE TREATMENT OR PREVENTION OF HEREDITARY ANGIOEDEMA
The present disclosure relates to methods of treating or preventing hereditary angioedema (HAE) in a subject in need thereof by subcutaneously administering to the subject an effective amount an anti-FXII antibody comprising (i) a V.sub.H comprising a CDRH1 comprising a sequence set forth in SEQ ID NO:1; a CDRH2 comprising a sequence set forth in SEQ ID NO:2; and a CDRH3 comprising a sequence set forth in SEQ ID NO:3; and (ii) a V.sub.L comprising a CDRL1 comprising a sequence set forth in SEQ ID NO:4; a CDRL2 comprising a sequence set forth in SEQ ID NO:5; and a CDRL3 comprising a sequence set forth in SEQ ID NO:6.
MicroRNA (miRNA) and Downstream Targets for Diagnostic and Therapeutic Purposes
In some embodiments, the invention is directed to a method for diagnosing fibrosis and/or fibrosis related diseases and to a method for screening a pharmaceutically active compound for the treatment of fibrosis and/or fibrosis related diseases. The present invention further relates to compositions for use in the treatment, amelioration, and/or prevention of fibrosis. In certain embodiments, the compositions modulate the activity of a miRNA for the treatment, amelioration, and/or prevention of fibrosis. In certain embodiments, the compositions inhibit the activity of miR-21 for the treatment, amelioration, and/or prevention of fibrosis.
COMPOSITION FOR TREATING DIABETIC RETINOPATHY, COMPRISING RAAV CONTAINING SOLUBLE VEGFR-1 VARIANT CDNA
The present invention provides a pharmaceutical composition for treating diabetic retinopathy. According to the present invention, the pharmaceutical composition can treat diabetic retinopathy by means of a single administration and thus, compared to conventional treatment methods, which require intraocular injection on a monthly basis, can reduce pain and ocular damage and infections in patients and reduce treatment costs.
INTRAOCULAR PRESSURE REDUCTION WITH INTRACAMERAL BIMATOPROST IMPLANTS
The present invention provides a method of treating an ocular condition in an eye of a patient, comprising the step of placing a biodegradable intraocular implant in an eye of the patient, the implant comprising a prostamide and a biodegradable polymer matrix that releases drug at a rate effective to sustain release of an amount of the prostamide from the implant to provide an amount of the prostamide effective to prevent or reduce a symptom of an ocular condition of the eye, wherein said ocular condition is elevated IOP and said implant is placed in an intracameral location to dilate the outflow channels of the eye emanating from Schlemm's Canal.
Methods of inhibiting serum glucocorticoid induced kinase 1 (SGKI) as a treatment for salt and water balance diseases
Methods of using serum glucocorticoid induced kinase 1 (SGK1) inhibitors for reducing the development of diseases related to salt and water balance, and in particular, hydrocephalus and/or hypertension, are disclosed herein. Particularly, the present disclosure is directed to the use of SGK1 inhibitors to inhibit transepithelial ion transport, such as in one embodiment, in the choroid plexus of a subject, thereby reducing cerebrospinal fluid (CSF) production or, alternatively, in another embodiment, to inhibit transepithelial sodium transport in the kidney collecting duct thereby reducing sodium reabsorption into the blood.