Described herein are modified fibroblast growth factors (FGFs), pharmaceutical compositions, ophthalmic formulations, and medicaments that include such modified FGFs, and methods of using such modified FGFs to treat ocular diseases, disorders, or conditions.

Engineered FGF1 and FGF2 polypeptides, polynucleotides encoding these polypeptides and DNA constructs, vectors and compositions including these engineered polypeptides are provided herein. The engineered FGF1 and FGF2 polypeptides are more stable than their wild-type counterparts and may be more effective at treating a variety of conditions that FGF1 and FGF2 are useful for treating such as wound healing.

Engineered FGF1 and FGF2 polypeptides, polynucleotides encoding these polypeptides and DNA constructs, vectors and compositions including these engineered polypeptides are provided herein. The engineered FGF1 and FGF2 polypeptides are more stable than their wild-type counterparts and may be more effective at treating a variety of conditions that FGF1 and FGF2 are useful for treating such as wound healing.

Described herein are modified fibroblast growth factors (FGFs), pharmaceutical compositions, ophthalmic formulations, and medicaments that include such modified FGFs, and methods of using such modified FGFs to treat ocular diseases, disorders, or conditions.

The present disclosure provides FGF1 mutant proteins, which selectively bind to/activate FGFR1b. Also provided are nucleic acid molecules that encode such proteins, and vectors and cells that include such nucleic acids. Methods of using the disclosed FGF1 mutants to reduce blood glucose in a mammal and treat a metabolic disorder are provided.

Methods of using FGF1 analogs, such as FGF1 mutant proteins having an N-terminal deletion, point mutation(s), or combinations thereof, to reduce blood glucose levels in subjects with steroid-induced diabetes, hypercortisolemia, or diabetes due to treatment with an antipsychotic agent, are provided. Such mutant FGF1 proteins can be part of a chimeric protein that includes a -Klotho-binding protein, an FGFR1-binding protein, a -Klotho-binding protein and a FGFR1-binding protein, a C-terminal region from FGF19 or FGF21.

Described herein are modified fibroblast growth factor (FGF) polypeptides, pharmaceutical compositions and medicaments that include such modified FGF polypeptides, and methods of using such modified FGF polypeptides to treat or prevent conditions that benefit from administration of FGFs.

The present disclosure provides FGF1 mutant proteins having one or more mutations in the heparin binding domain. Such mutants may also have an N-terminal deletion, point mutation(s), or combinations thereof. In some examples, the mutant FGF1 proteins have reduced mitogenic activity. Also provided are nucleic acid molecules that encode such proteins, and vectors and cells that include such nucleic acids. The disclosed FGF1 mutants can reduce blood glucose in a mammal, and in some examples are used to treat a metabolic disorder.

Engineered FGF1 and FGF2 polypeptides, polynucleotides encoding these polypeptides and DNA constructs, vectors and compositions including these engineered polypeptides are provided herein. The engineered FGF1 and FGF2 polypeptides are more stable than their wild-type counterparts and may be more effective at treating a variety of conditions that FGF1 and FGF2 are useful for treating such as wound healing.

The present disclosure provides FGF1 mutant proteins, which include an N-terminal deletion, point mutation(s), or combinations thereof, as well as FGF1-vagus targeting chimeric proteins which include an FGF1 portion (e.g., native FGF1 or mutant FGF1) and a portion that targets the chimera to the vagus nerve (e.g., GLP or exendin-4). Also provided are nucleic acid molecules that encode such proteins, and vectors and cells that include such nucleic acids. The disclosed FGF1 mutants and FGF1-vagus targeting chimeric proteins can reduce blood glucose in a mammal, and in some examples are used to treat a metabolic disorder.