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Biotech / Medical : Indications -- Cancer -- Ignore unavailable to you. Want to Upgrade?


To: Biomaven who wrote (30)4/17/2001 10:26:29 PM
From: Miljenko Zuanic  Respond to of 1840
 
<<It's a little weird that it specifically relates to a combo of an anti-neoplastic agent and Mab but excludes the conjugate. I assume there must have been prior art? At very first glance it doesn't cover the ABGX antibody itself, but seems to if the latter were to be used in conjunction with an anti-neoplastic agent.>>

Important words are:

"A method for inhibiting ...", not "A composition ..."

Claims specifically mentioned doxorubicin and cisplatin (not ALL or ANY cytostatic agent) as well as antibody 108 (and 96) produced by specific cell-line, not ANY mAb.

4. A method for inhibiting the growth of human tumor cells that express human EGF receptors and are mitogenically stimulated by human EGF according to claim 1 wherein said monoclonal antibody is 108 produced by hybridoma cell line ATCC HB 9764.

9. A therapeutic composition according to claim 6 wherein said monoclonal antibody is 108 produced by hybridoma cell line ATCC HB 9764.

I am not patent expert (not even amateur <g>), but it does not look to me as broad coverage of ANY combination of the ANY mAb and ANY cyostatic agent. Their (RPR) work date to 1988 (when initial application was first filed). So, IMCL PR issued 2 1/2 weeks before patent is issued sound TO ME as PURE HYPE. They licensed this RPR patent (at that time as application) because it covers method of the chimeric mAB production (special cell-line).

Miljenko

SUMMARY OF THE INVENTION

The present invention provides for novel hybridoma cell lines, ATCC HB 9763 and 9764, each of which provides as a component of the supernatant of its growth the highly specific monoclonal antibody, 96 and 108, respectively. Cell lines ATCC HB 9763 and 9764 were deposited in the American Type Culture Collection, 12301 Parklawn Drive, Rockville, Md. 20852, a recognized public depository for strains of microorganisms on Jul. 25, 1988. The present invention provides cell lines to produce novel monoclonal antibodies which inhibit the growth of human tumor cells that express human EGF receptor by binding specifically to the EGF receptor found on the cell membrane of the tumor cells.

An object of this invention is to provide two cell lines, each of which produces a novel monoclonal antibody that inhibits the growth of human tumor cells by the antibody binding to the extra-cellular domain of the human EGF receptors of the tumor cells in an antigen-antibody complex, wherein the tumor cells are characterized by their expression of human EGF receptors and mitogenic stimulation by EGF. The monoclonal antibodies are further characterized by their capability to inhibit the growth of either human oral epidermoid carcinoma (KB) cells or human mammary epithelial (184) cells by binding to the extra-cellular domain of the human EGF receptor of the KB or 184 cells in an antigen-antibody complex.

A further object of the invention is to provide a method for inhibiting the growth of human tumor cells that express human EGF receptors and are mitogenically stimulated by human EGF comprising administering an effective amount of a monoclonal antibody to a human cancer patient having said tumor cells whereby the antibody binds to the extra-cellular domain of the human EGF receptor of the tumor cell in an antigen-antibody complex, and the monoclonal antibody being further characterized by its capability of inhibiting the growth of either 184 or KB cells.

The invention further comprises a therapeutic composition comprising a pharmaceutical carrier in association with an effective amount of either one of the novel monoclonal antibodies to inhibit the growth of human tumor cells that express human EGF receptors and are mitogenically stimulated by human EGF.

Applicant has also surprisingly discovered that the combined treatment of one of the novel monoclonal antibodies with anti-neoplastic drugs such as doxorubicin or cisplatin provides a more efficient treatment for inhibiting the growth of human cancer cells that express human EGF receptors and are mitogenically stimulated by human EGF than the use of the novel monoclonal antibody or the anti-neoplastic agent by itself. The combined treatment using applicant's novel monoclonal antibodies is advantageous because it combines two anti-cancer agents, each operating via a different mechanism of action to yield a cytotoxic response to human tumor cells. That approach could solve problems arising in the clinic, such as, on the one hand, the development of resistance to drugs, and on the other hand, a change in the antigenicity of the tumor cells that would render them unreactive with the antibody. Furthermore, applicant has also surprisingly discovered that the anti-neoplastic agent can be administered at levels substantially lower than the levels required when administering the antineoplastic agent by itself, which are toxic or sub-toxic to the patient. Anti-neoplastic agents other than doxorubicin or cisplatin such as bleomycin sulfate, carmustine, chlorambucil, and cyclophosphamide hydroxyurea may also be used with the novel monoclonal antibody. The aforementioned list is merely exemplary and is not intended to limit the scope of the invention.

Thus, a further object of this invention provides a method for inhibiting the growth of human tumor cells that express human EGF receptors and are mitogenically stimulated by human EGF comprising administering an effective amount of an anti-neoplastic agent and an effective amount of either one of the novel monoclonal antibodies to a human cancer patient having said tumor cells, whereby the antibody binds to the extra-cellular domain of the human EGF receptor of the tumor cell in an antigen-antibody complex.

A further object of this invention provides a therapeutic composition comprising an effective amount of either one of the novel monoclonal antibodies and anti-neoplastic agent to inhibit the growth of human tumor cells that express human EGF receptors and are mitogenically stimulated by human EGF in association with a pharmaceutical carrier.