[5] The amino acid sequence of human noggin is highly homologous to that of rat, mouse, and Xenopus (an aquatic frog genus).

[9] Experiments in mice have shown that noggin also plays a role in learning, cognition,[10] bone development,[11] and neural tube fusion.

By diffusing through extracellular matrices more efficiently than members of the TGF-beta superfamily, noggin may have a principal role in creating morphogenic gradients.

A model knocking out Noggin specifically in adipocytes has allowed to elucidate that Noggin also plays a role in adipose tissue: its depletion in adipocytes causes alterations in the structure of both brown and white adipose tissue, along with brown fat dysfunction (impaired thermogenesis and β-oxidation) that results in dramatic increases of body weight and percent body fat that causes alterations in the lipid profile and in the liver; the effects vary with gender.

The formation of neural tissues, the notochord, hair follicles, and eye structures arise from the ectoderm germ layer.

Another craniofacial related deformity due to the absence of noggin is conductive hearing loss caused by uncontrolled outgrowth of the cochlear duct and coiling.

The discovery was based on the organism's ability to restore normal dorsal-ventral body axis in embryos that had been artificially ventralized by ultraviolet treatment.

Noggin was discovered in the laboratory of Richard M. Harland and William C. Smith at the University of California, Berkeley because of this ability to induce secondary axis formation in frog embryos.