Omalizumab

 ( Monoclonal Antibodies ) 

Limited studies are available to confirm whether omalizumab increases the risk of developing cardiovascular (CV) or cerebrovascular disease (CBV). Cohort and randomised controlled studies have shown that the risk of developing CV/CBV disease is around 20–32% higher in patients taking omalizumab compared to those not taking omalizumab. Additional multi-national, longitudinal studies with increased subject numbers are required to provide further clarification into the relationship and clinical significance between omalizumab and CV/CBV disease. Due to the severity of CV/CBVs side effects, clinicians and health care providers should continue to remain vigilant and monitor side effects when treating patients with omalizumab.

IgE may play an important role in the immune system's recognition of cancer cells. Therefore, indiscriminate blocking of IgE-receptor interaction with omalizumab may have unforeseen risks. The data pooled in 2003 from the earlier phase I to phase III clinical trials showed a numeric imbalance in malignancies arising in omalizumab recipients (0.5%) compared with control subjects (0.2%). A 2012 study found that a causal link with cancer was unlikely.

Tanox, a biopharmaceutical company based in Houston, Texas, started the anti-IgE program, created antibody drug candidates, and in 1987 filed its first patent application on the anti-IgE therapeutic approach. In 1988, the company converted one candidate antibody to a chimeric antibody (which was later named CGP51901 and further developed into a humanized antibody, TNX-901 or talizumab). The anti-IgE therapeutic concept was not well received in the early period of the program. Representatives of Ciba-Geigy (which merged with Sandoz to form Novartis in 1996) thought the anti-IgE program scientifically interesting and executives from Tanox and Ciba-Geigy signed a collaborative agreement in 1990 to develop the anti-IgE program.Development and Licensing Agreement, between Tanox and Ciba-Geigy 1990.

In 1991, after several rounds of pre-IND ("investigational new drug") meetings with officials/scientists of the FDA, the FDA finally allowed CGP51901 to be tested in human subjects. This approval of IND for an anti-IgE antibody for the first time was regarded a brave demonstration of professionalism for both the FDA officials and the Tanox/Ciba-Geigy team. The scientists participating in the pre-IND discussion comprehended that an ordinary anti-IgE antibody (i.e., one without the set of the binding specificity of CGP51901) would invariably activate mast cells and basophils and cause anaphylactic shock and probably deaths among injected persons. Notwithstanding this concern, they came to the same view that based on the presented scientific data, CGP51901 should have an absolutely required clean distinction from an ordinary anti-IgE antibody in this regard. In 1991–1993, researchers from Ciba-Geigy and Tanox and a leading clinical research group (headed by Stephen Holgate) in the asthma/allergy field ran a successful Phase I human clinical trial of CGP51901 in Southampton, England, and showed that the tested antibody is safe. In 1994–1995, the Tanox/Ciba-Geigy team conducted a Phase II trial of CGP51901 in patients with severe allergic rhinitis in Texas and showed that CGP51901 is safe and efficacious in relieving allergic symptoms.

While the Tanox/Ciba-Geigy anti-IgE program was gaining momentum, Genentech announced in 1993 that it also had an anti-IgE program for developing antibody therapeutics for asthma and other allergic diseases. Scientists in Genentech had made a mouse anti-IgE monoclonal antibody with the binding specificity similar to that of CGP51901 and subsequently humanized the antibody (the antibody was later named "omalizumab"). This caused great concerns in Tanox, because it had disclosed its anti-IgE technology and sent its anti-IgE antibody candidate, which was to become CGP51901 and TNX-901, to Genentech in 1989 for the latter to evaluate for the purpose of considering establishing a corporate partnership. Having failed to receive reconciliation from Genentech, Tanox filed a lawsuit against Genentech for trade secret violation. Coincidentally, Tanox started to receive major patents for its anti-IgE invention from the European Union and from the U.S. in 1995.The family of anti-IgE patents. ; ; ; ; . After a 3-year legal entanglement, Genentech and Tanox settled their lawsuits out-of-court and Tanox, Novartis, and Genentech formed a tripartite partnership to jointly develop the anti-IgE program in 1996.Tripartite Cooperation Agreement, by and between NOVARTIS PHARMA AG, GENENTECH, INC, AND TANOX, INC. Omalizumab became the drug of choice for further development, because it had a better developed manufacturing process than TNX-901. A large number of corporate-sponsored clinical trials and physician-initiated case series studies on omalizumab have been planned and performed since 1996 and a large number of research reports, especially those of clinical trial results, have been published since around 2000, as described and referenced in other sections of this article. In 2007, Genentech bought Tanox at $20/share for approximately $900 Million.

In October 2005, EMA issued the marketing authorization for omalizumab for the therapeutic indication of obstructive airway disease to Novartis.

The FDA approval of omalizumab for food allergy in February 2024 was based on the OUtMATCH trial, a randomized, double-blinded, placebo-controlled study that evaluated its efficacy and safety in those allergic to peanut and two other foods, including milk, egg, wheat, cashew, hazelnut, or walnut. The FDA granted the application breakthrough therapy designation.

in the United States, omalizumab cost about  to $4,600 per month.