Regeneron Pharmaceuticals, Inc.

Regeneran Pharmaceuticals, Inc.

Vincent J Idone

Aris N Economides

Sarah Jane Hatsell

Lori C Morton

Christopher Schoenherr

Sarah J Hatsell

Aris Economides

A genetically modified rodent is provided that comprises a modified Acvr1 gene that comprises a conditional altered exon 7 encoding R258G in antisense orientation, flanked by site-specific recombinase recognition sites, wherein the altered exon is inverted to sense orientation upon action of a recombinase, resulting in ectopic bone formation.

Nucleic acids comprising a modified rodent activin a receptor type 1 (Acvr1) gene

The present invention provides monoclonal antibodies that bind to the Activin A type I receptor (ACVR1) protein, and methods of use thereof. In various embodiments of the invention, the antibodies are fully human antibodies that bind to ACVR1. In some embodiments, the antibodies of the invention are useful for inhibiting ACVR1-mediated bone morphogenetic protein (BMP) signal transduction, thus providing a means of treating or preventing a disease, disorder or condition associated with ACVR1.

Anti-ACVR1 antibodies and uses thereof

The present invention provides antibodies that bind to human gremlin-1 (GREM1), and methods of use. According to certain embodiments of the invention, the antibodies are fully human antibodies that bind to GREM1. The antibodies of the invention are useful for inhibiting or neutralizing GREM1 activity, thus providing a means of treating a GREM1-related disease or disorder such as fibrosis and cancer. In some embodiments, the antibodies of the present invention are used in treating at least one symptom or complication of fibrosis of the liver, lungs or kidney.

Human antibodies to GREM1

A genetically modified rodent is provided that comprises a modified Acvr1 gene that comprises a conditional altered exon 7 encoding R258G in anti sense orientation, flanked by site-specific recombinase recognition sites, wherein the altered exon is inverted to sense orientation upon action of a recombinase, resulting in ectopic bone formation.

Genetically modified rodent with an inducible ACVR1 mutation in exon 7 that causes ectopic bone formation

Methods for treating Fibrodysplasia Ossificans Progressiva (FOP) are provided. Such methods involve administering to a subject having FOP an effective regime of an activin receptor type 2A (ACVR2A) and/or an activin receptor type 2B (ACVR2B) antagonist or an activin receptor type 1 (ACVR1) antagonist. Antagonists include fusion proteins of one or more extracellular domains (ECDs) of ACVR2A, ACVR2B and/or ACVR1 and the Fc domain of an immunoglobulin heavy chain, and antibodies against ACVR2A, ACVR2B, ACVR1 or Activin A.

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Ridgefield, CT, United States of America

Vincent J Idone