DR. JODIE LYNN BABITT, MD
Osteopathic Medicine in Boston, MA
License number
Massachusetts 205636
Category
Osteopathic Medicine
Type
Internal Medicine
License number
Massachusetts 205636
Category
Osteopathic Medicine
Type
Nephrology
Address
Address
55 Massachusetts General Hospital, Boston, MA 02114
Phone
(617) 726-5050
(617) 724-1122 (Fax)
(617) 724-0287
(617) 726-2894 (Fax)
(617) 724-1122 (Fax)
(617) 724-0287
(617) 726-2894 (Fax)
Professional information
Jodie Lynn Babitt, Boston MA
Specialties:
Internal Medicine, Nephrology
Work:
Richard B Simches Research Center
185 Cambridge St, Boston, MA 02114 Massachusetts General Hospital
55 Fruit St, Boston, MA 02114
185 Cambridge St, Boston, MA 02114 Massachusetts General Hospital
55 Fruit St, Boston, MA 02114
Education:
Harvard University(1999)
Jodie Lynn Babitt, Boston MA
Specialties:
Nephrologist
Address:
55 Fruit St, Boston, MA 02114
Education:
Doctor of Medicine
Board certifications:
American Board of Internal Medicine Certification in Internal Medicine, American Board of Internal Medicine Sub-certificate in Nephrology (Internal Medicine)
Dr. Jodie L Babitt - MD (Doctor of Medicine)
Hospitals:
55 Fruit St, Boston 02114
Massachusetts General Hospital
55 Fruit St, Boston 02114
55 Fruit St, Boston 02114
Massachusetts General Hospital
55 Fruit St, Boston 02114
Massachusetts General Hospital
55 Fruit St, Boston 02114
55 Fruit St, Boston 02114
Massachusetts General Hospital
55 Fruit St, Boston 02114
Education:
Medical Schools
Harvard Medical School
Graduated: 1999
Harvard Medical School
Graduated: 1999
Methods And Compositions To Regulate Iron Metabolism
US Patent:
2008026, Oct 23, 2008
Filed:
Feb 16, 2006
Appl. No.:
11/884509
Inventors:
Herbert Y. Lin - Watertown MA, US
Jodie Babitt - Brighton MA, US
Raymond T. Chung - Chestnut Hill MA, US
Tarek A. Samad - Princeton NJ, US
Alan L. Schneyer - Concord MA, US
Clifford J. Woolf - Newton MA, US
Jodie Babitt - Brighton MA, US
Raymond T. Chung - Chestnut Hill MA, US
Tarek A. Samad - Princeton NJ, US
Alan L. Schneyer - Concord MA, US
Clifford J. Woolf - Newton MA, US
Assignee:
THE GENERAL HOSPITAL CORPORATION - BOSTON MA
International Classification:
A61K 39/395, A61P 3/02
US Classification:
4241341
Abstract:
The present invention provides new systems and strategies for the regulation of iron metabolism in mammals. In particular, methods of using agonists and antagonists of TGF-β superfamily members to modulate the expression or activity of hepcidin, a key regulator of iron metabolism, are described. The inventive methods find applications in the treatment of diseases associated with iron overload, such as juvenile hemochromatosis and adult hemochromatosis, and in the treatment of diseases associated with iron deficiency, such as anemia of chronic disease and EPO resistant anemia in end-stage of renal disease. The present invention also relates to screening tools and methods for the development of novel drugs and therapies for treating iron metabolism disorders.
Soluble Tgf-B Type Iii Receptor Fusion Proteins
US Patent:
2007018, Aug 9, 2007
Filed:
May 7, 2004
Appl. No.:
10/556098
Inventors:
Herbert Lin - Watertown MA, US
Elisabetta Del Re - Concord MA, US
William Crowley - Newtonville MA, US
Jodie Babitt - Brighton MA, US
Elisabetta Del Re - Concord MA, US
William Crowley - Newtonville MA, US
Jodie Babitt - Brighton MA, US
International Classification:
A61K 39/395, C07H 21/04, C12P 21/06, C12N 5/06, C07K 16/22
US Classification:
424145100, 435069100, 435320100, 435336000, 530388250, 536023530
Abstract:
Soluble fusion proteins of the TGF-β type III receptor and novel methods for their production are disclosed herein for the first time. The fusion proteins of the invention competitively inhibit the binding of members of the TGF-β superfamily to their cell-surface receptors. Also provided are methods for using these fusion proteins to modulate the biological activity of members of the TGF-β superfamily under in vitro or in vivo conditions, and to prevent or treat a variety of pathophysiological conditions associated with overproduction of TGF-β or mediated by altered signaling pathways of the inhibin/activin system.