Patent ID: 11874283
Assignee: MOREHOUSE SCHOOL OF MEDICINE
Field: Pharmaceuticals (Chemistry)
Classification: CPC G  A  C | IPC A  C  G

Claim 3:
4. A method of monitoring the effectiveness of a treatment for IgA nephropathy directly linked to increased levels of ET-1 compared to ET-1 levels in those without IgA nephropathy, in a mammalian subject in need thereof and diagnosed at a qualified medical center as having said IgA nephropathy, comprising the steps of:
(a) administering to a subject with IgA nephropathy directly linked to increased levels of ET-1 compared to ET-1 levels in those without IgA nephropathy, in a mammalian subject in need thereof and diagnosed at a qualified medical center as having said IgA nephropathy, a pharmaceutical composition comprising:
(1) an active ingredient consisting of an ET-1 antagonist; and
(2) a pharmaceutically acceptable carrier,
wherein the active ingredient is the only active ingredient in the pharmaceutical composition and wherein the ET-1 antagonist is selected from the group consisting of sitaxentan, ambrisentan, atrasentan, BQ-123, bosentan and tezosentan;
(b) performing a first measurement of an ET-1-associated biomarker in a first biological sample from the subject, wherein the first biological sample is harvested prior to the initiation of the treatment in step (a);
(c) comparing the first measurement of an ET-1-associated biomarker to a control subject;
(d) performing a second measurement of the ET-1-associated biomarker in a second biological sample from the subject, wherein the second biological sample is harvested after the initiation of the treatment in step (a);
and
(e) determining the effectiveness of treatment for IgA nephropathy directly linked to increased levels of ET-1, based on the results from step (d) in comparison to step (b) as to the level of ET-1 as the ET-1-associated biomarker and adjusting the amount of ET-1 inhibitor administration based thereon; and separately determining the effect of treatment for IgA nephropathy directly linked to increased levels of ET-1, based on the results from step (d) in comparison to step (b) as to the level of any one or more ET-1-associated biomarkers selected from the group consisting of preproendothelin (ppET-1), proendothelin-1 (pET-1), BIG ET-1, endothelin converting enzyme (ECE), cystatin C, creatinine and albumin-creatinine ratio (ACR), and adjusting the amount of ET-1 inhibitor administration based thereon.