Changing the Treatment Paradigm in Cancer and Fibrotic Disease

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BLR Bio is a privately held biotechnology company committed to the discovery and development of transformational biologics and diagnostics for the treatment of Cancer and a broad spectrum of serious Fibrotic Diseases.

The majority of deaths in the developed world are due some fibroproliferative disease. It is now recognized that the pathways to fibrosis are not greatly different than those responsible for the formation of solid tumors. In fact, the formaton of a fibrotic-like cancer stroma and microenvironment is necessary for tumor survival, spread and resistance to both the immune targeting and chemotherapies. We have capitalized on this knowledge to develop a platform of diagnostics and theraputics targeting pathways common to both.

Our library of “first in class” biomolecules and peptides work through a novel approach to regulate key CCN signaling pathways, leveraging the company’s world leading expertise in the field of matricellular signaling molecules.

Our capabilities span drug discovery to Phase 3 clinical trials. We anticipate that our product candidates will be partnered with pharmaceutical or biotechnology companies for advanced development. We endeavor to retain a participating role applying our development and commercialization capabilities.

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© BLR Bio, L.L.C. | 313 54th Street, Kenosha, WI, USA, 53140 |

Latest News

May 2016
"Dr. Bruce Riser, CEO of BLR Bio, was an invited speaker on Peptide Discovery, Preclinical and Clinical presented at the TIDES Oligonucleotide and Peptide Therapeutics Conference, at Long Beach. See selected pre-interview."

April 2016
"BLR Bio was selected as one of the top 50 emerging biotechnology companies to present at the MedCity INVEST, Health Tech Showcase in Chicago April 10-12."

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April 2016
Balanced Regulation of the CCN Family of Matricellular Proteins: A Novel Approach to the Prevention and Treatment of Fibrosis and Cancer.
Journal of Cell Communication and Signaling 9.4 (2015): 327–339.
PMC. Web. 28 Apr. 2016.

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