Growth factors are polypeptides that stimulate cell proliferation and cell differentiation. They are major regulatory proteins controlling cell growth and cell signaling. They do this by a variety of mechanisms. Mostly, growth factors act as regulatory signals, similar to hormones. They can be either growth inhibitors or growth stimulators. Growth stimulators can stimulate cell migration, differentiation, and proliferation. Growth inhibitors can inhibit cell migration, inhibit invasion of tumor cells, and cause apoptosis. The growth factors are rate limiting, meaning when their supplies are exhausted, growth comes to a halt or slows drastically. There are many types of growth factors like EGFs, FGFs, hormones, insulin and insulin-like, PDGFs, TGFs, TNFs, and VEGFs. These growth factors can be produced by genetic engineering and used in aspects of science and medicine. For instance, growth factors are used in chemotherapy and cancer treatment to boost the patient’s white blood cell or platelet count. Conversely, growth factors can be exploited by cancer cells in order to facilitate rapid proliferation, cancer growth, and bodily cancer defense inhibition. Growth factor antibodies can bind against growth factors to inhibit them, facilitate them, or otherwise act against the growth factor to change its mechanism of action.

Anti-BMP5 antibody binds against the target bone morphogenetic protein 5. BMP 5 induces cartilage and bone formation. BMP5 is secreted by cells and expressed in the lung and liver. BMPs may also play a role in certain cancers. Anti-FGFR2 antibody binds against the target fibroblast growth factor receptor 2. FGFR2 is a receptor for acidic and basic fibroblast growth factors. Fibroblast growth factor receptor 2 is localized on the cell membrane of cells and is also secreted. Defects in FGFR2 are the cause of Crouzon syndrome, Apert syndrome, Pfeiffer syndrome, and familial scaphocephaly syndrome. Crouzon syndrome, also known as branchial arch syndrome, is a genetic disorder in which some of the skull bones fuse together prematurely which prevents normal skull growth. Affected individuals have distinct facial features like bulging eyes, a beaked nose, and underdeveloped jaws. Apert syndrome is similar to Crouzon syndrome. It is a genetic disorder that causes the skull bones to close earlier than normal and affects the shape of the head and face. Affected individuals may often also have fused fingers and fused toes. Pfeiffer syndrome and familial scaphocephaly syndrome, as well, have facial and cranial symptoms similar to those affected with Crouzon syndrome and branchial arch syndrome. Anti-BMPR1A antibody binds against bone morphogenetic protein receptor type 1A. BMPR1A forms a receptor complex consisting of four transmembrane serine/threonine kinases. BMPR1A is localized in the cell membrane and expressed in the skeletal muscle. Defects in bone morphogenetic protein receptor type 1A are the cause of juvenile polyposis syndrome and hereditary mixed polyposis syndrome 2. Juvenile polyposis syndrome is characterized by the multiple polyps in the gastrointestinal tract of a child or young adult. These polyps arise from abnormal growths in the mucous membrane. Hereditary mixed polyposis syndrome 2 is a very rare inherited cancer predisposition syndrome characterized by a considerable amount of polyps in the large intestine and rectum which causes many of the affected individuals to develop colorectal cancer.