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Researchers Submit Patent Application, "Method for Treating Ifnalpha Related Conditions", for Approval

February 10, 2014



By a News Reporter-Staff News Editor at AIDS Weekly -- From Washington, D.C., NewsRx journalists report that a patent application by the inventors Grouard-Vogel, Geraldine (Paris, FR); Dhellin, Olivier (Paris, FR); Fanget, Bernard (Chateauneuf, FR); Vandepapeliere, Pierre (Bonnine, BE); Roucairol, Camille (Paris, FR), filed on April 4, 2012, was made available online on January 30, 2014 (see also Biotechnology Companies).

The patent's assignee is Neovacs.

News editors obtained the following quote from the background information supplied by the inventors: "The IFN type I family includes IFN.alpha., IFN.beta., IFN.delta., IFN1, IFN.kappa., IFN.tau., and IFN .omega.. The predominant forms are IFN.alpha., of which 13 closely related proteins are described in humans, and the single IFN.beta.. Despite the fact that different IFN type I forms may promote different biological responses, all IFN type I are structurally related (their genes lack introns and are located on the short arm of chromosome 9) and signal through the same receptor subunits (Van Boxel-Dezaire et al., Immunity 2006; 25:361-372).

"The interest on the relationship between IFN type I and autoimmune disorders is nowadays increasing, since the signs of its induction, the so-called interferon signature, have been recently reported in patients suffering from different autoimmune diseases (Baccala et al. Immunol Rev 2005; 204:9-26). In fact, due to its immune-modulator effects, IFN type I seems to be involved in several pathogenic pathways of various autoimmune conditions.

"The paradigm of IFN type I pathogenic relevance in autoimmunity is systemic lupus erythematosus (SLE). SLE is a chronic disease, characterized by a multi-organ involvement, due to a paradoxical damage of organs caused by autoantibodies directed to self-antigens. The etiology of SLE is complex, involving both genetic and environmental factors. The serum level of IFN.alpha. in SLE has been shown to correlate with the severity of the disease (Dall'era et al. Ann Rheum Dis 2005; 64:1692-7). Sjogren's syndrome (SS), also known as sicca syndrome, is a chronic, systemic, autoimmune condition which affects the exocrine glands, particularly the salivary and lachrymal glands. Elevated IFN.alpha. activity has also been observed in the serum of patients suffering from this disease. Finally, other conditions such as diabetes, rheumatoid arthritis, scleroderma, vasculitis and autoimmune thyroiditis have also been shown to be associated with high levels of IFN.alpha.

"Sedaghat et al. also recently suggested that type 1 IFN may play a role in CD4.sup.+ T cells depletion in HIV.sup.+ patients as they showed that type 1 IFN affect the steady state of normal CD4.sup.+ T cells dynamics by shifting the balance towards Th1 effectors that are short lived cells instead of long-lived memory T cells (Sedaghat et al. J. Virol. 2008, 82(4): 1870-1883). This was confirmed in Mandl et al., where it is suggested to diminish the IFN.alpha. production by plasmacytoid dendritic cells to ameliorate the pathological immune activation (Mandl et al. Nat. Med. 2008).

"Moreover, administration of IFN.alpha. has been reported to exacerbate underlying disease in patients with psoriasis, autoimmune thyroiditis and multiple sclerosis and to induce an SLE like syndrome in patients without a previous history of autoimmune disease.

"Therefore, there is a need for an agent that inhibits IFN.alpha. activity.

"Passive immunization with monoclonal neutralizing antibodies is currently being tested in clinical trials with rontalizumab and sifalimumab for the treatment of SLE. However, said therapy presents the drawbacks of targeting only one subset of the 13 for IFN.alpha. and the use of passively administrated monoclonal antibodies can be limited by the induction of anti-drug antibodies. Said anti-drug antibodies may neutralize or otherwise compromise the clinical effect of the drugs and can also be associated with serious adverse events related to cross-reactivity with autologous proteins (De Groot et al. Trends. Immunol. 2007, 28(11)).

"The present invention thus provides a method for inhibiting IFN.alpha. activity in vivo by administering a therapeutically effective amount of an immunogenic product that allows an active immunization which can break immunological B cell tolerance and generate high titers of polyclonal neutralizing antibodies against IFN.alpha. and its use for treating IFN.alpha. related conditions."

As a supplement to the background information on this patent application, NewsRx correspondents also obtained the inventors' summary information for this patent application: "One object of the invention is an immunogenic product comprising IFN.alpha. coupled to a carrier protein molecule for use in preventing or treating an IFN.alpha. related condition in a subject in need thereof, wherein the therapeutically effective amount of the immunogenic product to be administrated to the subject is more than 30 mcg of immunogenic product per administration, preferably at least 60 mcg.

"In one embodiment of the invention, the administration of the therapeutically effective amount of the immunogenic product prevents the occurrence of symptoms of a disease linked to an over-production of IFN.alpha.

"In another embodiment of the invention, the administration of the therapeutically effective amount of the immunogenic product prevents the flare of a disease linked to an over-production of IFN.alpha.

"In another embodiment of the invention, the IFN.alpha. related conditions comprise systemic lupus erythematosus, rheumatoid arthritis, scleroderma, Sjogren syndrome, vasculitis, HIV, type I diabetes, autoimmune thyroiditis and myositis.

"In another embodiment of the invention, the therapeutically effective amount of the immunogenic product to be administrated to the subject is from 35 mcg to 1000 mcg of immunogenic product per administration, preferably from 60 mcg to 1000 mcg.

"In another embodiment of the invention, the immunogenic product is administrated to the subject at least twice in a month.

"In another embodiment of the invention, the immunogenic product is further administrated to the subject at least once every three months.

"In another embodiment of the invention, the immunogenic product is further administrated to the subject when, in a serum sample obtained from the subject, the amount of anti-IFN.alpha. antibodies is undetectable.

"In another embodiment of the invention, the immunogenic product is strongly inactivated, which means that the product shows less than 5% of antiviral activity in the conditions of TEST B.

"In another embodiment of the invention, the immunogenic product is capable of neutralizing the antiviral activity of IFN.alpha. in the conditions of TEST C.

"In another embodiment of the invention, the immunogenic product comprises at least one subtype of IFN.alpha.

"In another embodiment of the invention, the subtype of IFN.alpha. is IFN.alpha. 2b and the carrier protein molecule is KLH.

"In another embodiment of the invention, the immunogenic product is a vaccine, preferably in the form of an emulsion.

"Another object of the invention is a unit dosage form comprising more than 30 mcg of an immunogenic product comprising IFN.alpha. coupled to a carrier protein molecule as defined here above.

"Another object of the invention is a medical device comprising more than 30 mcg of an immunogenic product comprising IFN.alpha. coupled to a carrier protein molecule as defined here above.

"Another object of the invention is a kit comprising at least one vial containing more than 30 mcg, preferably at least 60 mcg, of an immunogenic product comprising IFN.alpha. coupled to a carrier protein molecule as defined here above, at least one vial containing adjuvant, and means for contacting said immunogenic product to the adjuvant, and for emulsifying the mixture of the aqueous solution with the adjuvant.

"In one embodiment, the kit of the invention comprises at least one vial containing more than 30 mcg, preferably at last 60 mcg, of an immunogenic product comprising IFN.alpha. coupled to a carrier protein molecule according to the invention, and means for solubilizing said immunogenic product, preferably in an aqueous solution, or at least one vial containing a solution preferably an aqueous solution, comprising more than 30 mcg, preferably at least 60 mcg, of an immunogenic product comprising IFN.alpha. coupled to a carrier protein molecule according to the invention, and at least one vial containing adjuvant, and means for contacting said solution to the adjuvant, and for emulsifying the mixture of the solution with the adjuvant."

For additional information on this patent application, see: Grouard-Vogel, Geraldine; Dhellin, Olivier; Fanget, Bernard; Vandepapeliere, Pierre; Roucairol, Camille. Method for Treating Ifnalpha Related Conditions. Filed April 4, 2012 and posted January 30, 2014. Patent URL: http://appft.uspto.gov/netacgi/nph-Parser?Sect1=PTO2&Sect2=HITOFF&u=%2Fnetahtml%2FPTO%2Fsearch-adv.html&r=2661&p=54&f=G&l=50&d=PG01&S1=20140123.PD.&OS=PD/20140123&RS=PD/20140123

Keywords for this news article include: Neovacs, Genetics, Immunology, CD Antigens, Thyroiditis, CD4 Antigens, Therapeutics, HIV Receptors, Blood Proteins, Differentiation, Immunoglobulins, Serum Globulins, Carrier Proteins, Membrane Proteins, Biological Factors, Autoimmune Diseases, Autoimmune Disorders, T-Lymphocyte Antigens, Biotechnology Companies.

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Source: AIDS Weekly


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