Tanox started the "anti-IgE therapy" program and developed a prototype antibody candidate in 1987, and subsequently converted the mouse antibody candidate into a chimeric form and obtained crucial set of data on the antibody in 1988–89. The Tanox' anti-IgE antibodies were designed to target free IgE in blood and IgE-expressing B lymphocytes for the purpose of intercepting the IgE-mediated pathway, without binding to IgE already bound by the high affinity IgE receptors on mast cells and basophils or bound by the low-affinity IgE receptors on many cell types. An ordinary anti-IgE antibody, if were injected into a patient, would cause a massive activation of mast cells and basophils and hence anaphylactic shocks. By 1989, Tanox had collected data showing that their proposed therapeutic lead anti-IgE antibody could not induce the activation of basophils isolated from the blood of any of many extremely allergic individuals, even under the most permissive conditions.