32 results about "Autosomal dominant polycystic kidney disease" patented technology

Disclosed are methods for treating kidney disease including autosomal dominant polycystic kidney disease (ADPKD) in a subject, comprising the step of administering to the subject a composition comprising a therapeutically effective amount of ticagrelor or a derivative thereof, thereby treating ADPKD. Disclosed are methods of decreasing arginine vasopressin (AVP) production in a subject comprising the step of administering to the subject a composition comprising an effective amount of ticagrelor, thereby decreasing AVP production. Disclosed are methods for treating dilutional hyponatremia in a subject comprising the step of administering to the subject a composition comprising an effective amount of ticagrelor, thereby decreasing AVP production.

Provided herein are methods for the treatment of polycystic kidney disease, including autosomal dominant polycystic kidney disease, using modified oligonucleotides targeted to miR-17.

Provided herein are methods for the treatment of poly-cystic kidney disease, including autosomal dominant polycystic kidney disease, using modified oligonucleotides targeted to miR-17.

Provided herein are methods for the treatment of polycystic kidney disease, including autosomal dominant polycystic kidney disease, using modified oligonucleotides targeted to miR-17.

Compounds of formula (I), wherein the groups are as defined in the specification, are very useful for the preparation of medicaments for the treatment of cardiovascular disorders, especially heart failure and hypertension. These compounds are inhibitors of the enzymatic activity of Na+, K+-ATPases. They are very useful for the manufacture of medicaments for the treatment of diseases caused by the hypertensive effects of endogenous ouabain, such as progression of renal failure in autosomal dominant polycystic kidney disease (ADPKD), preeclamptic hypertension and protein Urine and renal failure progression in patients with adducin polymorphisms.

Methods for treating autosomal dominant polycystic kidney disease (ADPKD) are described herein. More particularly, methods described herein relate generally to administering glutaminase1 inhibitors to subjects afflicted with ADPKD. Accordingly, the use and application of compounds or agents that inhibit glutaminase1 for treating ADPKD or for use in a medicament for treating ADPKD are encompassed herein.

The invention relates to the application of pyrimidine (thio) ketone compounds in the preparation of medicines for treating secretory diarrhea and autosomal dominant hereditary polycystic kidney disease. Cystic fibrosis transmembrane conductance regulator is a Cl-channel protein activated by cyclic adenosine monophosphate. During the design of the model, multiple activation pathways of CFTR were considered, and multiple activation pathways were combined to screen During the process, it binds at the Cl-transport channel. The application of pyrimidine (thio) ketone compounds in the preparation of drugs for treating secretory diarrhea and autosomal dominant polycystic kidney disease is screened on the basis of screening a large number of compounds by using the model for screening inhibitors directly combined with CFTR. It can effectively prevent and treat the occurrence of swine diarrhea. Effectively inhibits fluid secretion from epithelial cells lining autosomal dominant polycystic kidney cysts. The inhibitory effect is rapid, and there is no obvious toxic effect.

The invention provides the application of 1-indanone in the preparation of medicine for treating or preventing autosomal dominant polycystic kidney disease. The present invention uses the MDCK vesicle model to prove that 1-indanone can inhibit the formation and growth of vesicles, and determines the renal pharmacological activity of 1-indanone through the in vitro embryonic kidney vesicle model, which has a significant effect on the development of vesicles in the kidney. Finally, it was further proved in the polycystic kidney mouse model that 1-indanone also had the effect of inhibiting the occurrence and development of vesicles in vivo. The above-mentioned vesicle inhibitory effects in vitro and in vivo showed a dose-effect relationship.