Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
DETAILED ACTION
Claims 2-20 are currently pending and under prosecution.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
Claim(s) 2-5 and 13-19 are rejected under 35 U.S.C. 103 as being unpatentable over De Weers et al (US20090148449 A1; Published 6/11/2009), in view of Cespedes et al (“Daratumumab, a Novel Human Anti-CD38 Monoclonal Antibody for the Treatment of Chronic Lymphocytic Leukemia and B-Cell Non–Hodgkin Lymphoma”, Blood, 642. CLL - Therapy, excluding Transplantation: Poster III, vol 120, issue 21, 11/2012, pg 3935) and Fisher et al (“Comparison of a Standard Regimen (CHOP) with Three Intensive Chemotherapy Regimens for Advanced Non-Hodgkin's Lymphoma”, N Engl J Med 1993;328:1002-1006).
It is noted that the instant specification discloses the following:
Daratumumab is an example of the anti-CD38 antibody encompassed by claim 2.
The sequences of Daratumumab (SEQ ID Nos: 4-11) is disclosed on pages 13-16 of the instant specification, and comparison with sequences demonstrates it includes these CDRs from the claims.
De Weers et al teaches a method of treating non-Hogdkin’s lymphoma, comprising administering to a subject an anti-CD38 antibody comprising: a heavy chain complementarity determining region (HCDR1), HCDR2, and HCDR3 amino acid sequences and light chain complementarity determining region LCDR1-3 that match 100% to the instantly claimed sequences. See sequence alignments below. [1027-1028, 1030, 1031] De Weers teaches that the antibody may be combined with multiple agents which act by different mechanisms to induce apoptosis. [1010] De Weers teaches that the anti-CD38 antibody may be combined with at least one chemotherapeutic agent. [1078] De Weers teaches that these chemotherapeutic agents may include cyclophosphamide, doxorubicin, and vincristine. [1079-1081, 1138] De Weers further teaches that the therapeutic agent may be combined with a corticosteroid, such as prednisone. [1095-1096]
Regarding claims 3 and 17, De Weers teaches that the anti-CD38 antibody induces killing of CD38-expressing cells by ADCC, [0065] and by CDC [0066]. Regarding claims 4 and 18, De Weers teaches that the anti-CD38 antibody is of IgG1 isotype. [0073, 0601, 0951] Regarding claims 5 and 19, Weers teaches that the anti-CD38 antibody comprises a heavy chain variable region (VH) of SEQ ID NO: 17, which matches 100% to the instantly claimed SEQ ID NO: 4 and a light chain variable region (VL) of SEQ ID NO: 12, which matches 100% to instantly claimed SEQ ID NO: 5. See sequence alignments below. Regarding claims 13 and 14, De Weers teaches that this combination therapy may be administered simultaneously, sequentially, or separately. [1071] Regarding claim 15, De Weers teaches that the subject is further treated with radiotherapy. [1119-1122] Regarding claim 16, De Weers teaches that the NHL treated may be follicular lymphoma [FL], mantle-cell lymphoma (MCL), Burkitt’s lymphoma, or diffuse large B-cell lymphoma [1028]
However, Weers does not demonstrate the specific combination comprising anti-CD38 antibody and CHOP.
SEQUENCE ALIGNMENTS
SEQ ID Nos: 6-7-8
RESULT 3
US-11-886-932A-17
(NOTE: this sequence has 4 duplicates in the database searched)
Sequence 17, US/11886932A
Patent No. 7829673
GENERAL INFORMATION
APPLICANT: DE WEERS, MICHEL
APPLICANT: GRAUS, YVO
APPLICANT: OPRINS, JUDITH
APPLICANT: PARREN, PAUL
APPLICANT: VAN DE WINKEL, JAN
APPLICANT: VAN VUGT, MARTINE
TITLE OF INVENTION: ANTIBODIES AGAINST CD38 FOR TREATMENT OF MULTIPLE MYELOMA
FILE REFERENCE: GMI-083US
CURRENT APPLICATION NUMBER: US/11/886,932A
CURRENT FILING DATE: 2009-12-24
PRIOR APPLICATION NUMBER: PCT/DK2006/000166
PRIOR FILING DATE: 2006-03-23
PRIOR APPLICATION NUMBER: 60/728,561
PRIOR FILING DATE: 2005-10-20
PRIOR APPLICATION NUMBER: 60/696,163
PRIOR FILING DATE: 2005-07-01
PRIOR APPLICATION NUMBER: 60/667,579
PRIOR FILING DATE: 2005-04-01
PRIOR APPLICATION NUMBER: DK PA 200500429
PRIOR FILING DATE: 2005-03-23
NUMBER OF SEQ ID NOS: 71
SEQ ID NO 17
LENGTH: 124
TYPE: PRT
ORGANISM: Homo sapiens
Query Match 86.9%; Score 163.4; Length 124;
Best Local Similarity 43.2%;
Matches 35; Conservative 0; Mismatches 0; Indels 46; Gaps 2;
Qy 1 SFAM--------------SAISGSGGGTYYADSVKG------------------------ 22
|||| ||||||||||||||||||
Db 31 SFAMSWVRQAPGKGLEWVSAISGSGGGTYYADSVKGRFTISRDNSKNTLYLQMNSLRAED 90
Qy 23 --------DKILWFGEPVFDY 35
|||||||||||||
Db 91 TAVYFCAKDKILWFGEPVFDY 111
SEQ ID NOS: 9-10-11
RESULT 12
US-11-886-932A-12
(NOTE: this sequence has 80 duplicates in the database searched)
Sequence 12, US/11886932A
Patent No. 7829673
GENERAL INFORMATION
APPLICANT: DE WEERS, MICHEL
APPLICANT: GRAUS, YVO
APPLICANT: OPRINS, JUDITH
APPLICANT: PARREN, PAUL
APPLICANT: VAN DE WINKEL, JAN
APPLICANT: VAN VUGT, MARTINE
TITLE OF INVENTION: ANTIBODIES AGAINST CD38 FOR TREATMENT OF MULTIPLE MYELOMA
FILE REFERENCE: GMI-083US
CURRENT APPLICATION NUMBER: US/11/886,932A
CURRENT FILING DATE: 2009-12-24
PRIOR APPLICATION NUMBER: PCT/DK2006/000166
PRIOR FILING DATE: 2006-03-23
PRIOR APPLICATION NUMBER: 60/728,561
PRIOR FILING DATE: 2005-10-20
PRIOR APPLICATION NUMBER: 60/696,163
PRIOR FILING DATE: 2005-07-01
PRIOR APPLICATION NUMBER: 60/667,579
PRIOR FILING DATE: 2005-04-01
PRIOR APPLICATION NUMBER: DK PA 200500429
PRIOR FILING DATE: 2005-03-23
NUMBER OF SEQ ID NOS: 71
SEQ ID NO 12
LENGTH: 107
TYPE: PRT
ORGANISM: Homo sapiens
Query Match 82.8%; Score 119.3; Length 107;
Best Local Similarity 37.3%;
Matches 28; Conservative 0; Mismatches 0; Indels 47; Gaps 2;
Qy 1 RASQSVSSYLA---------------DASNRAT--------------------------- 18
||||||||||| |||||||
Db 24 RASQSVSSYLAWYQQKPGQAPRLLIYDASNRATGIPARFSGSGSGTDFTLTISSLEPEDF 83
Qy 19 -----QQRSNWPPTF 28
||||||||||
Db 84 AVYYCQQRSNWPPTF 98
SEQ ID NO: 4
RESULT 3
US-11-886-932A-17
(NOTE: this sequence has 4 duplicates in the database searched)
Sequence 17, US/11886932A
Patent No. 7829673
GENERAL INFORMATION
APPLICANT: DE WEERS, MICHEL
APPLICANT: GRAUS, YVO
APPLICANT: OPRINS, JUDITH
APPLICANT: PARREN, PAUL
APPLICANT: VAN DE WINKEL, JAN
APPLICANT: VAN VUGT, MARTINE
TITLE OF INVENTION: ANTIBODIES AGAINST CD38 FOR TREATMENT OF MULTIPLE MYELOMA
FILE REFERENCE: GMI-083US
CURRENT APPLICATION NUMBER: US/11/886,932A
CURRENT FILING DATE: 2009-12-24
PRIOR APPLICATION NUMBER: PCT/DK2006/000166
PRIOR FILING DATE: 2006-03-23
PRIOR APPLICATION NUMBER: 60/728,561
PRIOR FILING DATE: 2005-10-20
PRIOR APPLICATION NUMBER: 60/696,163
PRIOR FILING DATE: 2005-07-01
PRIOR APPLICATION NUMBER: 60/667,579
PRIOR FILING DATE: 2005-04-01
PRIOR APPLICATION NUMBER: DK PA 200500429
PRIOR FILING DATE: 2005-03-23
NUMBER OF SEQ ID NOS: 71
SEQ ID NO 17
LENGTH: 124
TYPE: PRT
ORGANISM: Homo sapiens
Query Match 100.0%; Score 643; Length 124;
Best Local Similarity 100.0%;
Matches 122; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 EVQLLESGGGLVQPGGSLRLSCAVSGFTFNSFAMSWVRQAPGKGLEWVSAISGSGGGTYY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 EVQLLESGGGLVQPGGSLRLSCAVSGFTFNSFAMSWVRQAPGKGLEWVSAISGSGGGTYY 60
Qy 61 ADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYFCAKDKILWFGEPVFDYWGQGTLVTV 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 ADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYFCAKDKILWFGEPVFDYWGQGTLVTV 120
Qy 121 SS 122
||
Db 121 SS 122
SEQ ID NO: 5
RESULT 1
US-11-886-932A-12
(NOTE: this sequence has 80 duplicates in the database searched)
Sequence 12, US/11886932A
Patent No. 7829673
GENERAL INFORMATION
APPLICANT: DE WEERS, MICHEL
APPLICANT: GRAUS, YVO
APPLICANT: OPRINS, JUDITH
APPLICANT: PARREN, PAUL
APPLICANT: VAN DE WINKEL, JAN
APPLICANT: VAN VUGT, MARTINE
TITLE OF INVENTION: ANTIBODIES AGAINST CD38 FOR TREATMENT OF MULTIPLE MYELOMA
FILE REFERENCE: GMI-083US
CURRENT APPLICATION NUMBER: US/11/886,932A
CURRENT FILING DATE: 2009-12-24
PRIOR APPLICATION NUMBER: PCT/DK2006/000166
PRIOR FILING DATE: 2006-03-23
PRIOR APPLICATION NUMBER: 60/728,561
PRIOR FILING DATE: 2005-10-20
PRIOR APPLICATION NUMBER: 60/696,163
PRIOR FILING DATE: 2005-07-01
PRIOR APPLICATION NUMBER: 60/667,579
PRIOR FILING DATE: 2005-04-01
PRIOR APPLICATION NUMBER: DK PA 200500429
PRIOR FILING DATE: 2005-03-23
NUMBER OF SEQ ID NOS: 71
SEQ ID NO 12
LENGTH: 107
TYPE: PRT
ORGANISM: Homo sapiens
Query Match 100.0%; Score 556; Length 107;
Best Local Similarity 100.0%;
Matches 107; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 EIVLTQSPATLSLSPGERATLSCRASQSVSSYLAWYQQKPGQAPRLLIYDASNRATGIPA 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 EIVLTQSPATLSLSPGERATLSCRASQSVSSYLAWYQQKPGQAPRLLIYDASNRATGIPA 60
Qy 61 RFSGSGSGTDFTLTISSLEPEDFAVYYCQQRSNWPPTFGQGTKVEIK 107
|||||||||||||||||||||||||||||||||||||||||||||||
Db 61 RFSGSGSGTDFTLTISSLEPEDFAVYYCQQRSNWPPTFGQGTKVEIK 107
Cespedes teaches a method of treating non-Hogdkin’s lymphoma (NHL) in a subject, comprising administering to the subject: an anti-CD38 antibody, daratumumab. Regarding claims 3 and 16, Cespedes teaches that daratumumab induces killing of tumor cells via complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC). Regarding claim 17, Cespedes teaches the use of daratumumab in two types of B-cell NHL, follicular lymphoma (FL) and mantle cell lymphoma (ML). Cespedes teaches that CD38 is important for cell migration and adhesion and that daratumumab is a promising therapeutic agent. [Whole Abstract]
Fisher et al teaches a method of treating non-Hodgkin’s lymphoma comprising administering CHOP (cyclophosphamide, doxorubicin, vincristine). Fisher also teaches that CHOP has cured ~ 30% of patients with advanced stages of intermediate-grade or high-grade non-Hogdkin’s lymphoma. [Abstract]
It would have been prima facie obvious to one of ordinary skill in the art at the time the invention was filed to combine the instantly claimed anti-CD38 antibody and CHOP for the treatment of non-Hodgkin’s lymphoma. One would have been motivated to, and have a reasonable expectation of success because: (1) De Weers and Cespedes both teaches methods of treating non-Hogdkin’s lymphoma, comprising administering to a subject the instantly claimed anti-CD38 antibody, (2) De Weers teaches that the antibody may be combined with multiple agents which act by different mechanisms to induce apoptosis, and that these agents may be at least one chemotherapeutic agent, including cyclophosphamide, doxorubicin, and vincristine, as well as prednisone, (3) Cespedes teaches that CD38 is important for cell migration and adhesion and that daratumumab is a promising therapeutic agent, (4) Fisher et al teaches a method of treating non-Hodgkin’s lymphoma comprising administering CHOP (cyclophosphamide, doxorubicin, vincristine) and demonstrates the efficacy of this combination.
Those of skill in the art recognize that the these agents, anti-CD38 antibody and CHOP, are all known to successfully, pharmaceutically treat non-Hodgkin’s lymphoma, could have been combined by known methods, and that in combination, each agent of the composition merely would have performed the same function as they did separately, and one of ordinary skill in the art would have recognized that the results of the combination would predictably treat NHL and have additive effects through the combination of the all of the agents.
As stated in the above rejection, each of these agents had been taught by the prior art to be effective at treating NHL, thus the instant situation is amenable to the type of analysis set forth in In re Kerkhoven, 205 USPQ 1069 (CCPA 1980) wherein the court held that: “It is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition which is to be used for the very same purpose. In re Susi, 58 CCPA 1074, 1079-80, 440 F.2d 442, 445, 169 USPQ 423, 426 (1971); In re Crockett, 47 CCPA 1018, 1020-21, 279 F.2d 274, 276-77, 126 USPQ 186, 188 (1960). As this court explained in Crockett, the idea of combining them flows logically from their having been individually taught in the prior art.” In the instant case, it is prima facie obvious to combine all of the agents (anti-CD38 antibody + CHOP) each of which is taught by the prior art to be useful for the same purpose, in order to form the composition which is to be used for the very same purpose of treating non-Hodgkin’s lymphoma.
Claim(s) 7-12 are rejected under 35 U.S.C. 103 as being unpatentable over De Weers et al (US20090148449 A1; Published 6/11/2009), Cespedes et al (“Daratumumab, a Novel Human Anti-CD38 Monoclonal Antibody for the Treatment of Chronic Lymphocytic Leukemia and B-Cell Non–Hodgkin Lymphoma”, Blood, 642. CLL - Therapy, excluding Transplantation: Poster III, vol 120, issue 21, 11/2012, pg 3935) and Fisher et al (“Comparison of a Standard Regimen (CHOP) with Three Intensive Chemotherapy Regimens for Advanced Non-Hodgkin's Lymphoma”, N Engl J Med 1993;328:1002-1006), as applied to claims 2-5 and 13-19 above, and further in view of LeJeune et al (US20110293606 A1; Published 12/1/2011), de Weers et al (2) (Daratumumab, a Novel Therapeutic Human CD38 Monoclonal Antibody, Induces Killing of Multiple Myeloma and Other Hematological Tumors, The Journal of Immunology, Volume 186, Issue 3, February 2011, Pages 1840–1848), and Rezvani, (“Rituximab resistance.” Best practice & research. Clinical haematology vol. 24,2 (2011): 203-16).
The teachings of De Weers, Cespedes and Fisher are taught above. However, these references do not teach the limitations of claims 7-12:
Claim 7. The method of claim 2, wherein the subject: a) is resistant to or has acquired resistance to treatment with at least one chemotherapeutic agent or a combination of at least one chemotherapeutic agent and an anti-CD20 antibody; b) has discontinued treatment with at least one chemotherapeutic agent or a combination of at least one chemotherapeutic agent and an anti-CD20 antibody due to side effects, or both a) and b).
Claim 8. The method of claim 7, wherein the anti-CD20 antibody is rituximab, ofatumumab, veltuzumab, ocrelizumab, obinutuzumab (GA-101), PRO13192 or ocratuzumab (AME-133v).
Claim 9. The method of claim 8, wherein the anti-CD20 antibody is rituximab.
Claim 10. The method of claim 7, wherein the at least one chemotherapeutic agent comprises cyclophosphamide, doxorubicin, vincristine, prednisone, ifosfamide, carboplatin, etoposide, or a combination of the foregoing.
Clam 11. The method of claim 10, wherein the at least one chemotherapeutic agent comprises a combination of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).
Claim 12. The method of claim 10, wherein the at least one chemotherapeutic agent comprises a combination of ifosfamide, carboplatin, and etoposide (ICE).
LeJeune teaches a method treating non-Hodgkin’s lymphoma in a subject, comprising administering to the subject: a) an anti-CD38 antibody, and b) vincristine. LeJeune teaches that this combination allows for therapeutic synergy. LeJeune teaches that this method may be used to treat Burkitt’s lymphoma. [0023, 0038] LeJeune teaches that this method is useful for treating cancers that are resistant to the commonly used anti-cancer agents as the anti-CD38 antibodies of the invention have a unique mechanism of action. [0038]
De Weers (2) teaches that targeted immunotherapy with monoclonal antibodies has become critical for the successful treatment of many forms of cancer. De Weers teaches that anti-CD38 antibody, daratumumab, was found effective in killing tumor cells by ADCC and CDC. De Weers demonstrated the effects of daratumumab in drug-resistant cell lines and demonstrated that this antibody is active in areas which usually supports tumor growth, survival and development of drug resistance. [pg 1847, Conclusion, 1st column]
Rezvani teaches that rituximab is a vital component of therapy for follicular non-Hogdkin’s lymphoma, and while effective, it is limited by treatment resistance. teaches mechanisms to rituximab resistance, including resistance to CDC, ADCC and apoptosis. [pgs 6-8] Rezvani teaches ways to overcome resistance is to enhance ADCC and CDC proteins and pathways. [pg 10]
It is noted that claims 7-12 require that the method of claim 2, wherein the subject is resistant to or has acquired resistance to treatment with at least one chemotherapeutic agent or a combination of at least one chemotherapeutic agent and an anti-CD20 antibody. This limitation would have been obvious to those of ordinary skill in the art, because: (1) De Weers and Cespedes both teaches methods of treating non-Hogdkin’s lymphoma, comprising administering to a subject the instantly claimed anti-CD38 antibody, (2) LeJeune taches a method of treating non-Hodgkin’s lymphoma comprising administering an anti-CD38 antibody and vincristine, and teaches that this method is useful for treating cancers that are resistant to the commonly used anti-cancer agents as the anti-CD38 antibodies of the invention have a unique mechanism of action, (3) Fisher teaches that anti-cancer agents that are used to treat this cancer type include CHOP, (4) Rezvani teaches that rituximab, which is a known anti-CD20 antibody, used for treatment of non-Hodgkin’s lymphoma, is limited in its use due to resistance pathways, including in CDC and ADCC pathways, (5) De Weers (2) teaches and demonstrates the effects of daratumumab in drug-resistant cell lines and demonstrated that this antibody is active in areas which usually supports tumor growth, survival and development of drug resistance.
Given the recognized need to treatment resistant non-Hodgkin’s lymphoma, given the known mechanisms of resistance of known agents that treat non-Hodgkin’s lymphoma including chemotherapeutic agents and anti-CD20 antibodies, and given the known mechanism in which an anti-CD38 antibody is used and can be used to overcome resistance of these agents, one of skill in the art could have pursued treating a subject that is resistant or has acquired resistance to treatment with at least one chemotherapeutic agent or a combination of at least one chemotherapeutic agent and an anti-CD20 antibody, with a reasonable expectation of success.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 2-20 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-18 of U.S. Patent No. 9,603,927 in Although the claims at issue are not identical, they are not patentably distinct from each other because the U.S. Patent recites a method of treating a subject having a CD38-positive hematological malignancy, comprising administering to the subject in need thereof an anti-CD38 antibody in combination with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP), wherein the anti-CD38 antibody induces in vitro killing of CD38-expressing cells by antibody-dependent cell-mediated cytotoxicity (ADCC), antibody-dependent cellular phagocytosis (ADCP), complement dependent cytotoxicity (CDC), apoptosis, or in vitro modulation of CD38 enzymatic activity and comprises the instantly claimed sequences of the anti-CD38 antibody, wherein the subject is resistant to or has acquired resistance to treatment with at least one chemotherapeutic agent. The U.S. Patent recites that the CD38-positive hematological malignancy is non-Hodgkin’s lymphoma.
The referenced U.S. Patent and the instant application are claiming common subject matter, as follows:
Instant Application: 18/771,839
U.S. Patent: 9,603,927
Claim 2. A method of treating non-Hodgkin's lymphoma (NHL) in a subject in need thereof, comprising administering to the subject:
a) an anti-CD38 antibody comprising:
i) a heavy chain complementarity determining region 1 (HCDR1), a HCDR2 and a HCDR3 amino acid sequences of SEQ ID NOs: 6, 7 and 8, respectively; and
ii) a light chain complementarity determining region 1 (LCDR1), a LCDR2 and a LCDR3 amino acid sequences of SEQ ID NOs: 9, 10 and 11, respectively; and
b) cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).
Claim 3. The method of claim 2, wherein the anti-CD38 antibody induces killing of CD38-expressing cells by:
a) antibody-dependent cell-mediated cytotoxicity (ADCC);
b) antibody-dependent cellular phagocytosis (ADCP);
c) complement dependent cytotoxicity (CDC);
d) apoptosis;
e) modulation of CD38 enzymatic activity;
or a combination of the foregoing.
Claim 7. The method of claim 2, wherein the subject:
a) is resistant to or has acquired resistance to treatment with at least one chemotherapeutic agent or a combination of at least one chemotherapeutic agent and an anti-CD20 antibody;
b) has discontinued treatment with at least one chemotherapeutic agent or a combination of at least one chemotherapeutic agent and an anti-CD20 antibody due to side effects,
or both a) and b).
Claim 17. The method of claim 16, wherein the anti-CD38 antibody induces killing of CD38-expressing cells by:
a) antibody-dependent cell-mediated cytotoxicity (ADCC);
b) antibody-dependent cellular phagocytosis (ADCP);
c) complement dependent cytotoxicity (CDC);
d) apoptosis;
e) modulation of CD38 enzymatic activity;
or a combination of the foregoing.
Claim 1. A method of treating a subject having a CD38-positive hematological malignancy, comprising administering to the subject in need thereof an anti-CD38 antibody in combination with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP), wherein the anti-CD38 antibody induces in vitro killing of CD38-expressing cells by antibody-dependent cell-mediated cytotoxicity (ADCC), antibody-dependent cellular phagocytosis (ADCP), complement dependent cytotoxicity (CDC), apoptosis, or in vitro modulation of CD38 enzymatic activity and comprises heavy chain complementarity determining region (HCDR) 1 (HCDR1), 2 (HCDR2) and 3 (HCDR3) sequences of SEQ ID NOs: 6, 7 and 8, respectively, and light chain complementarity determining region (LCDR) 1 (LCDR1), 2 (LCDR2) and 3 (LCDR3) sequences of SEQ ID NOs: 9, 10 and 11, respectively, wherein the subject is resistant to or has acquired resistance to treatment with at least one chemotherapeutic agent.
Claim 2. The method of claim 1, wherein the anti-CD38 antibody induces killing of the CD38-expressing cells by ADCC or CDC in vitro.
Claim 4. The method of claim 2, wherein the anti-CD38 antibody is of IgG1 isotype.
Claim 18. The method of claim 16, wherein the anti-CD38 antibody is of IgG1 isotype.
Claim 5. The method of claim 2, wherein the anti-CD38 antibody comprises a heavy chain variable region (VH) of SEQ ID NO: 4 and a light chain variable region (VL) of SEQ ID NO: 5.
Claim 6. The method of claim 2, wherein the anti-CD38 antibody comprises a heavy chain of SEQ ID NO: 12 and a light chain of SEQ ID NO: 13.
Claim 19. The method of claim 16, wherein the anti-CD38 antibody comprises a heavy chain variable region (VH) of SEQ ID NO: 4 and a light chain variable region (VL) of SEQ ID NO: 5.
Claim 20. The method of claim 16, wherein the anti-CD38 antibody comprises a heavy chain of SEQ ID NO: 12 and a light chain of SEQ ID NO: 13.
Claim 3. The method of claim 2, wherein the anti-CD38 antibody is of IgG1, IgG2, IgG3 or IgG4 isotype.
Claim 6. The method of claim 1, wherein the anti-CD38 antibody comprises a heavy chain variable region (VH) of SEQ ID NO: 4 and a light chain variable region (VL) of SEQ ID NO: 5.
Claim 7. The method of claim 6, wherein the anti-CD38 antibody comprises a heavy chain of SEQ ID NO: 12 and a light chain of SEQ ID NO: 13.
Claim 8. The method of claim 7, wherein the anti-CD20 antibody is rituximab, ofatumumab, veltuzumab, ocrelizumab, obinutuzumab (GA-101), PRO13192 or ocratuzumab (AME-133v).
Claim 9. The method of claim 8, wherein the anti-CD20 antibody is rituximab.
Claim 10. The method of claim 7, wherein the at least one chemotherapeutic agent comprises cyclophosphamide, doxorubicin, vincristine, prednisone, ifosfamide, carboplatin, etoposide, or a combination of the foregoing.
Claim 11. The method of claim 10, wherein the at least one chemotherapeutic agent comprises a combination of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).
Claim 12. The method of claim 10, wherein the at least one chemotherapeutic agent comprises a combination of ifosfamide, carboplatin, and etoposide (ICE).
Claim 10. The method of claim 8, wherein the subject is resistant to or has acquired resistance to treatment with a combination of at least one chemotherapeutic agent and an anti-CD20 antibody.
Claim 11. The method of claim 8, wherein the subject has discontinued treatment with at least one chemotherapeutic agent or a combination of at least one chemotherapeutic agent and an anti-CD20 antibody due to side effects.
Claim 12. The method of claim 10 or 11, wherein the anti-CD20 antibody is rituximab (RITUXAN®), ofatumumab (ARZERRA®), veltuzumab, ocrelizumab, obinutuzumab (GA-101), PRO13192 or ocratuzumab (AME-133v).
Claim 13. The method of claim 12, wherein the anti-CD20 antibody is rituximab.
Claim 14. The method of claim 10 or 11, wherein the at least one chemotherapeutic agent is cyclophosphamide, doxorubicin, vincristine, prednisone, ifosfamide, carboplatin or etoposide
.
Claim 15. The method of claim 14, wherein the at least one chemotherapeutic agent is a combination of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP).
Claim 16. The method of claim 14, wherein the at least one chemotherapeutic agent is a combination of ifosfamide, carboplatin and etoposide (ICE).
Claim 13. The method of claim 2, wherein the anti-CD38 antibody, cyclophosphamide, doxorubicin, vincristine, and prednisone are administered simultaneously.
Claim 14. The method of claim 2, wherein the anti-CD38 antibody, cyclophosphamide, doxorubicin, vincristine and prednisone are administered sequentially or separately.
Claim 17. The method of claim 1, wherein the anti-CD38 antibody, cyclophosphamide, doxorubicin, vincristine and prednisone are administered simultaneously, sequentially or separately.
Claim 15. The method of claim 2, wherein the subject is further treated with radiotherapy.
Claim 18. The method of claim 1, wherein the patient is further treated with radiotherapy.
Claim 16. The method of claim 2, wherein the NHL is diffuse large B-cell lymphoma (DLBCL), Burkitt's lymphoma (BL), follicular lymphoma (FL), or mantle-cell lymphoma (MCL).
Claim 8. The method of claim 1, wherein the CD38-positive hematological malignancy is multiple myeloma, acute lymphoblastic leukemia (ALL), non-Hodgkin's lymphoma (NHL), diffuse large B-cell lymphoma (DLBCL), Burkitt's lymphoma (BL), follicular lymphoma (FL) or mantle-cell lymphoma (MCL).
Claim 9. The method of claim 8, wherein the CD38-positive hematological malignancy is DLBCL.
Claims 2-20 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-16 of U.S. Patent No. 10,800,851. Although the claims at issue are not identical, they are not patentably distinct from each other because the U.S. Patent recites a method of treating a subject having diffuse large B-cell lymphoma, comprising administering to the subject in need thereof an anti-CD38 antibody in combination with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP), wherein the anti-CD38 antibody induces in vitro killing of CD38-expressing cells by antibody-dependent cell-mediated cytotoxicity (ADCC), antibody-dependent cellular phagocytosis (ADCP), complement dependent cytotoxicity (CDC), apoptosis, or in vitro modulation of CD38 enzymatic activity and comprises the instantly claimed sequences of the anti-CD38 antibody
The referenced U.S. Patent and the instant application are claiming common subject matter, as follows:
Instant Application: 18/771,839
U.S. Patent: 10,800,851
Claim 2. A method of treating non-Hodgkin's lymphoma (NHL) in a subject in need thereof, comprising administering to the subject:
a) an anti-CD38 antibody comprising:
i) a heavy chain complementarity determining region 1 (HCDR1), a HCDR2 and a HCDR3 amino acid sequences of SEQ ID NOs: 6, 7 and 8, respectively; and
ii) a light chain complementarity determining region 1 (LCDR1), a LCDR2 and a LCDR3 amino acid sequences of SEQ ID NOs: 9, 10 and 11, respectively; and
b) cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).
Claim 3. The method of claim 2, wherein the anti-CD38 antibody induces killing of CD38-expressing cells by:
a) antibody-dependent cell-mediated cytotoxicity (ADCC);
b) antibody-dependent cellular phagocytosis (ADCP);
c) complement dependent cytotoxicity (CDC);
d) apoptosis;
e) modulation of CD38 enzymatic activity;
or a combination of the foregoing.
Claim 17. The method of claim 16, wherein the anti-CD38 antibody induces killing of CD38-expressing cells by:
a) antibody-dependent cell-mediated cytotoxicity (ADCC);
b) antibody-dependent cellular phagocytosis (ADCP);
c) complement dependent cytotoxicity (CDC);
d) apoptosis;
e) modulation of CD38 enzymatic activity;
or a combination of the foregoing.
Claim 16. The method of claim 2, wherein the NHL is diffuse large B-cell lymphoma (DLBCL), Burkitt's lymphoma (BL), follicular lymphoma (FL), or mantle-cell lymphoma (MCL).
Claim 1. A method of treating a subject having diffuse large B-cell lymphoma, comprising administering to the subject in need thereof an anti-CD38 antibody in combination with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP), wherein the anti-CD38 antibody induces in vitro killing of CD38-expressing cells by antibody-dependent cell-mediated cytotoxicity (ADCC), antibody-dependent cellular phagocytosis (ADCP), complement dependent cytotoxicity (CDC), apoptosis, or in vitro modulation of CD38 enzymatic activity and comprises a heavy chain complementarity determining region 1 (HCDR1), a HCDR2 and a HCDR3 amino acid sequences of SEQ ID NOs: 6, 7 and 8, respectively, and a light chain complementarity determining region 1 (LCDR1), a LCDR2 and a LCDR3 amino acid sequences of SEQ ID NOs: 9, 10 and 11, respectively.
Claim 2. The method of claim 1, wherein the anti-CD38 antibody induces killing of the CD38-expressing cells by ADCC or CDC in vitro.
Claim 4. The method of claim 2, wherein the anti-CD38 antibody is of IgG1 isotype.
Claim 18. The method of claim 16, wherein the anti-CD38 antibody is of IgG1 isotype.
Claim 5. The method of claim 2, wherein the anti-CD38 antibody comprises a heavy chain variable region (VH) of SEQ ID NO: 4 and a light chain variable region (VL) of SEQ ID NO: 5.
Claim 19. The method of claim 16, wherein the anti-CD38 antibody comprises a heavy chain variable region (VH) of SEQ ID NO: 4 and a light chain variable region (VL) of SEQ ID NO: 5.
Claim 6. The method of claim 2, wherein the anti-CD38 antibody comprises a heavy chain of SEQ ID NO: 12 and a light chain of SEQ ID NO: 13.
Claim 20. The method of claim 16, wherein the anti-CD38 antibody comprises a heavy chain of SEQ ID NO: 12 and a light chain of SEQ ID NO: 13.
Claim 3. The method of claim 2, wherein the anti-CD38 antibody is of IgG1, IgG2, IgG3 or IgG4 isotype.
Claim 6. The method of claim 1, wherein the anti-CD38 antibody comprises a heavy chain variable region (VH) of SEQ ID NO: 4 and a light chain variable region (VL) of SEQ ID NO: 5.
Claim 7. The method of claim 1, wherein the anti-CD38 antibody comprises a heavy chain of SEQ ID NO: 12 and a light chain of SEQ ID NO: 13.
Claim 7. The method of claim 2, wherein the subject:
a) is resistant to or has acquired resistance to treatment with at least one chemotherapeutic agent or a combination of at least one chemotherapeutic agent and an anti-CD20 antibody;
b) has discontinued treatment with at least one chemotherapeutic agent or a combination of at least one chemotherapeutic agent and an anti-CD20 antibody due to side effects,
or both a) and b).
Claim 8. The method of claim 1, wherein the subject is resistant to or has acquired resistance to treatment with at least one chemotherapeutic agent or a combination of at least one chemotherapeutic agent and an anti-CD20 antibody.
Claim 9. The method of claim 1, wherein the subject has discontinued treatment with at least one chemotherapeutic agent or a combination of at least one chemotherapeutic agent and an anti-CD20 antibody due to side effects.
Claim 8. The method of claim 7, wherein the anti-CD20 antibody is rituximab, ofatumumab, veltuzumab, ocrelizumab, obinutuzumab (GA-101), PRO13192 or ocratuzumab (AME-133v).
Claim 9. The method of claim 8, wherein the anti-CD20 antibody is rituximab.
Claim 10. The method of claim 7, wherein the at least one chemotherapeutic agent comprises cyclophosphamide, doxorubicin, vincristine, prednisone, ifosfamide, carboplatin, etoposide, or a combination of the foregoing.
Claim 11. The method of claim 10, wherein the at least one chemotherapeutic agent comprises a combination of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).
Claim 12. The method of claim 10, wherein the at least one chemotherapeutic agent comprises a combination of ifosfamide, carboplatin, and etoposide (ICE).
Claim 10. The method of claim 8 or 9, wherein the anti-CD20 antibody is rituximab (RITUXAN®), ofatumumab (ARZERRA®), veltuzumab, ocrelizumab, obinutuzumab (GA-101), PRO13192 or ocratuzumab (AME-133v).
Claim 11. The method of claim 10, wherein the anti-CD20 antibody is rituximab.
Claim 12. The method of claim 8 or 9, wherein the at least one chemotherapeutic agent is cyclophosphamide, doxorubicin, vincristine, prednisone, ifosfamide, carboplatin or etoposide.
Claim 13. The method of claim 12, wherein the at least one chemotherapeutic agent is a combination of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP).
Claim 14. The method of claim 12, wherein the at least one chemotherapeutic agent is a combination of ifosfamide, carboplatin and etoposide (ICE).
Claim 13. The method of claim 2, wherein the anti-CD38 antibody, cyclophosphamide, doxorubicin, vincristine, and prednisone are administered simultaneously.
Claim 14. The method of claim 2, wherein the anti-CD38 antibody, cyclophosphamide, doxorubicin, vincristine and prednisone are administered sequentially or separately.
Claim 15. The method of claim 1, wherein the anti-CD38 antibody, cyclophosphamide, doxorubicin, vincristine and prednisone are administered simultaneously, sequentially or separately.
Claim 15. The method of claim 2, wherein the subject is further treated with radiotherapy.
Claim 6. The method of claim 1, wherein the subject is further treated with radiotherapy.
Claims 2-20 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of U.S. Patent No. 12,060,432. Although the claims at issue are not identical, they are not patentably distinct from each other because the U.S. Patent recites a method of treating non-Hodgkin's lymphoma (NHL) in a subject in need thereof, comprising administering to the subject an anti-CD38 antibody in combination with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP), wherein: a) the NHL is diffuse large B-cell lymphoma (DLBCL), Burkitt's lymphoma (BL), follicular lymphoma (FL) or mantle-cell lymphoma (MCL), b) the anti-CD38 antibody induces in vitro killing of CD38-expressing cells by antibody-dependent cell-mediated cytotoxicity (ADCC), antibody-dependent cellular phagocytosis (ADCP), complement dependent cytotoxicity (CDC), apoptosis, or in vitro modulation of CD38 enzymatic activity, and c) the anti-CD38 antibody and comprises the instantly claimed sequences.
The referenced U.S. Patent and the instant application are claiming common subject matter, as follows:
Instant Application: 18/771,839
U.S. Patent:
Claim 2. A method of treating non-Hodgkin's lymphoma (NHL) in a subject in need thereof, comprising administering to the subject:
a) an anti-CD38 antibody comprising:
i) a heavy chain complementarity determining region 1 (HCDR1), a HCDR2 and a HCDR3 amino acid sequences of SEQ ID NOs: 6, 7 and 8, respectively; and
ii) a light chain complementarity determining region 1 (LCDR1), a LCDR2 and a LCDR3 amino acid sequences of SEQ ID NOs: 9, 10 and 11, respectively; and
b) cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).
Claim 16. The method of claim 2, wherein the NHL is diffuse large B-cell lymphoma (DLBCL), Burkitt's lymphoma (BL), follicular lymphoma (FL), or mantle-cell lymphoma (MCL).
Claim 3. The method of claim 2, wherein the anti-CD38 antibody induces killing of CD38-expressing cells by:
a) antibody-dependent cell-mediated cytotoxicity (ADCC);
b) antibody-dependent cellular phagocytosis (ADCP);
c) complement dependent cytotoxicity (CDC);
d) apoptosis;
e) modulation of CD38 enzymatic activity;
or a combination of the foregoing.
Claim 17. The method of claim 16, wherein the anti-CD38 antibody induces killing of CD38-expressing cells by:
a) antibody-dependent cell-mediated cytotoxicity (ADCC);
b) antibody-dependent cellular phagocytosis (ADCP);
c) complement dependent cytotoxicity (CDC);
d) apoptosis;
e) modulation of CD38 enzymatic activity;
or a combination of the foregoing.
Claim 1. A method of treating non-Hodgkin's lymphoma (NHL) in a subject in need thereof, comprising administering to the subject an anti-CD38 antibody in combination with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP), wherein:
a) the NHL is diffuse large B-cell lymphoma (DLBCL), Burkitt's lymphoma (BL), follicular lymphoma (FL) or mantle-cell lymphoma (MCL),
b) the anti-CD38 antibody induces in vitro killing of CD38-expressing cells by antibody-dependent cell-mediated cytotoxicity (ADCC), antibody-dependent cellular phagocytosis (ADCP), complement dependent cytotoxicity (CDC), apoptosis, or in vitro modulation of CD38 enzymatic activity, and
c) the anti-CD38 antibody comprises a heavy chain complementarity determining region 1 (HCDR1), a HCDR2 and a HCDR3 amino acid sequences of SEQ ID NOs: 6, 7 and 8, respectively, and a light chain complementarity determining region 1 (LCDR1), a LCDR2 and a LCDR3 amino acid sequences of SEQ ID NOs: 9, 10 and 11, respectively.
Claim 2. The method of claim 1, wherein the anti-CD38 antibody induces killing of the CD38-expressing cells by ADCC or CDC in vitro.
Claim 18. The method of claim 1, wherein the NHL is BL.
Claim 19. The method of claim 1, wherein the NHL is FL.
Claim 20. The method of claim 1, wherein the NHL is MCL.
Claim 4. The method of claim 2, wherein the anti-CD38 antibody is of IgG1 isotype.
Claim 18. The method of claim 16, wherein the anti-CD38 antibody is of IgG1 isotype.
Claim 5. The method of claim 2, wherein the anti-CD38 antibody comprises a heavy chain variable region (VH) of SEQ ID NO: 4 and a light chain variable region (VL) of SEQ ID NO: 5.
Claim 19. The method of claim 16, wherein the anti-CD38 antibody comprises a heavy chain variable region (VH) of SEQ ID NO: 4 and a light chain variable region (VL) of SEQ ID NO: 5.
Claim 6. The method of claim 2, wherein the anti-CD38 antibody comprises a heavy chain of SEQ ID NO: 12 and a light chain of SEQ ID NO: 13.
Claim 20. The method of claim 16, wherein the anti-CD38 antibody comprises a heavy chain of SEQ ID NO: 12 and a light chain of SEQ ID NO: 13.
Claim 3. The method of claim 2, wherein the anti-CD38 antibody is of IgG1, IgG2, IgG3 or IgG4 isotype.
Claim 6. The method of claim 1, wherein the anti-CD38 antibody comprises a heavy chain variable region (VH) of SEQ ID NO: 4 and a light chain variable region (VL) of SEQ ID NO: 5.
Claim 7. The method of claim 1, wherein the anti-CD38 antibody comprises a heavy chain of SEQ ID NO: 12 and a light chain of SEQ ID NO: 13.
Claim 7. The method of claim 2, wherein the subject:
a) is resistant to or has acquired resistance to treatment with at least one chemotherapeutic agent or a combination of at least one chemotherapeutic agent and an anti-CD20 antibody;
b) has discontinued treatment with at least one chemotherapeutic agent or a combination of at least one chemotherapeutic agent and an anti-CD20 antibody due to side effects,
or both a) and b).
Claim 8. The method of claim 1, wherein the subject is resistant to or has acquired resistance to treatment with at least one chemotherapeutic agent or a combination of at least one chemotherapeutic agent and an anti-CD20 antibody.
Claim 9. The method of claim 1, wherein the subject has discontinued treatment with at least one chemotherapeutic agent or a combination of at least one chemotherapeutic agent and an anti-CD20 antibody due to side effects.
Claim 8. The method of claim 7, wherein the anti-CD20 antibody is rituximab, ofatumumab, veltuzumab, ocrelizumab, obinutuzumab (GA-101), PRO13192 or ocratuzumab (AME-133v).
Claim 9. The method of claim 8, wherein the anti-CD20 antibody is rituximab.
Claim 10. The method of claim 7, wherein the at least one chemotherapeutic agent comprises cyclophosphamide, doxorubicin, vincristine, prednisone, ifosfamide, carboplatin, etoposide, or a combination of the foregoing.
Claim 11. The method of claim 10, wherein the at least one chemotherapeutic agent comprises a combination of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).
Claim 12. The method of claim 10, wherein the at least one chemotherapeutic agent comprises a combination of ifosfamide, carboplatin, and etoposide (ICE).
Claim 13. The method of claim 2, wherein the anti-CD38 antibody, cyclophosphamide, doxorubicin, vincristine, and prednisone are administered simultaneously.
Claim 14. The method of claim 2, wherein the anti-CD38 antibody, cyclophosphamide, doxorubicin, vincristine and prednisone are administered sequentially or separately.
Claim 10. The method of claim 8 or 9, wherein the anti-CD20 antibody is rituximab, ofatumumab, veltuzumab, ocrelizumab, obinutuzumab (GA-101), PRO13192 or ocratuzumab (AME-133v).
Claim 11. The method of claim 10, wherein the anti-CD20 antibody is rituximab.
Claim 12. The method of claim 8 or 9, wherein the at least one chemotherapeutic agent is cyclophosphamide, doxorubicin, vincristine, prednisone, ifosfamide, carboplatin or etoposide.
Claim 13. The method of claim 12, wherein the at least one chemotherapeutic agent is a combination of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP).
Claim 14. The method of claim 12, wherein the at least one chemotherapeutic agent is a combination of ifosfamide, carboplatin and etoposide (ICE).
Claim 15. The method of claim 1, wherein the anti-CD38 antibody, cyclophosphamide, doxorubicin, vincristine and prednisone are administered simultaneously.
Claim 17. The method of claim 1, wherein the anti-CD38 antibody, cyclophosphamide, doxorubicin, vincristine and prednisone are administered sequentially or separately.
Claim 15. The method of claim 2, wherein the subject is further treated with radiotherapy.
Claim 16. The method of claim 1, wherein the subject is further treated with radiotherapy.
Closest Prior Art
Claims 6 and 20 do not have prior art rejection, however, they have double patent rejection. These claims recite that the anti-CD38 antibody comprises a heavy chain of SEQ ID NO: 12 and a light chain of SEQ ID NO: 13. The closest prior art made of record is De Weers et al (US20090148449 A1; Published 6/11/2009). De Weers teaches an anti-CD38 antibody, However, does not teach that the anti-CD38 antibody comprises the sequences of the heavy chain (SEQ ID NO: 12) and light chain (SEQ ID NO: 13).
Conclusion
Conclusion: Claims 2-20 are rejected.
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/SARAH A ALSOMAIRY/ Examiner, Art Unit 1646
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