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
The office acknowledges Applicants filing of the claim amendments dated 7/13/2023. Claims 1-34 has been cancelled. Claims 37-39, 41-44, 46 have been amended. Claims 35-46 are pending and are examined based on the merits herein.
Application Priority
This application filed 07/13/2023 is a National Stage entry of PCT/EP2022/ 050891, International Filing Date: 01/17/2022, claims foreign priority to 21152018.4, filed 01/18/2021, claims foreign priority to 21201509.3, filed 10/07/2021, claims foreign priority to 21205665.9, filed 10/29/2021.
Information Disclosure Statement
The information disclosure statement(s) (IDS) filed on 7/13/2023 and 9/19/2024 are in compliance with the provisions of 37 CFR 1.97. Accordingly, the IDS is being considered by the Examiner.
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.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claim(s) 35-46 are rejected under 35 U.S.C. 103 as being unpatentable over Erikkson et al. (US 10300053) in view of Mondet (Molecules, 2021, 1323, p 1-16), Chen (Nature Medicine, 2019, 25, 103-110), and Veryaskina et al. (Medicina 2020, 56, 376, p 1-16).
Erikkson teach a method of treatment of acute myeloid leukemia by administration to a mammal in need thereof of 4-hydroxy-5-methoxy-N,1-dimethyl-2-oxo-N-[4-(trifluoromethyl)phenyl]-1,2-dihydroquinoline-3-carboxamide (aka tasquinimod) (See claim 1). Erikkson is explicit in teaching that the treatment is by oral administration, an amount ranging from 0.001 mg to 0.2 mg of the compound/kg of body weight per day, or of a corresponding amount of the pharmaceutically acceptable salt, by administration of the compound or salt 1-3 times a day, the compound is administered as solid dosage form, the solid dosage form is a tablet or capsule, the compound or salt is administered dissolved or suspended in a liquid vehicle, and the treatment further comprises radiation therapy and/or autologous stem cell transplantation (see claims 1-5, 7-15, 17-18).
Erikkson is not explicit in teaching the treatment of myelodysplastic syndrome with tasquinimod.
Mondet teach that deregulations of the expression of the S100A8 and S100A9 genes and/or proteins, as well as changes in their plasma levels or their levels of secretion in the bone marrow microenvironment, are frequently observed in acute myeloid leukemia (AML) (See Abstract, p 3, lines 1-5). The impact of S100A8 and S100A9 in disruption of hematopoiesis and leukemic progression is taught in Fig. 3. The reference teach different ways of targeting S100 A8 and/or S100A9 at different stages of development of acute leukemia. Tasquinimod targets the microenvironment by preventing interactions between TLR4, RAGE and S100A9 (See Fig. 4). Mondet further teach that circulating S100A8 and S100A9 homodimers and S100A8/A9 heterodimers is found in plasma of 30 myelodysplastic syndrome patients (See p 5, para 2). The reference teaches that ‘Chen et al. showed that the plasma concentration of S100A9 significantly increased in MDS patients and that, in a murine model of S100A9 expression, S100A9 derived expansion and activation of MDSC that contributed to cytopenia and myelodysplasia’ (See page 7, para 3). The impact of S100A8 and S100A9 proteins on hematopoietic microenvironment has been highlighted by a transcriptional analysis of mesenchymal cells (p 7, last two lines).
Chen is explicit in teaching that myelodysplastic syndromes (MDS) frequently progress to acute myeloid leukemia (Abstract). Chen teach that MDS are malignant, preleukemic, hematologic disorders with poor clinical outcome and a median overall survival of less than 2 years in higher-risk subtypes; The clonal origin of MDS and AML has been demonstrated to lie within the phenotypic and functionally defined stem cell compartment (See p 103, col. 1, para 1, lines 1-3, 6-8).
Veryaskina teach that myelodysplastic syndromes (MDS) are a group of clonal diseases of hematopoietic stem cells and are characterized by multilineage dysplasia in immature myeloid cells, ineffective hematopoiesis, peripheral blood cytopenias and a high risk of transformation to acute myeloid leukemia (AML). Also taught is that a retrospective analysis of 36,558 MDS cases revealed that the frequency of AML secondary to MDS was 3.7% in patients aged 40 years and under, and 2.5% in patients aged 40 years and over (See p 1, para 1, Introduction, lines 1-5). The reference teaches that chronic myelomonocytic leukemia (CMML) is one of the subtypes of AML (See Table 2). Veryaskina teach that the International Prognostic Scoring System (IPSS) separates MDS patients into four different risk subgroups: low, intermediate-1, intermediate-2 and high (See p 7, 5.1, para 2, lines 3-4).
From the teachings of Mondet, Chen and Veryaskina it would have been obvious to a skilled artisan before the effective filing date of the invention that (i) changes in the expression levels of S100A8 and S100A9 proteins are observed both in acute myeloid leukemia and MDS (ii) tasquinimod targets the microenvironment by preventing interactions between TLR4, RAGE and S100A9 and (iii) myelodysplastic syndromes (MDS) progress to acute myeloid leukemia. Erikkson is explicit in teaching the use of tasquinimod in acute myeloid leukemia. A person skilled in the art from the combined prior art teachings would have found it obvious to treat subjects with MDS with tasquinimod. A person skilled in the art would have been motivated to treat MDS with a reasonable amount of success and derive therapeutic effects. As to the limitation of therapeutically effective amount, Erikkson teach an amount ranging from 0.001 mg to 0.2 mg of the compound/kg of body weight per day of tasquinimod in treating AML. Thus a skilled artisan would have found it obvious to administer the same amount to treat MDS in subjects. Thus claims 35 and 37 are addressed.
As to claims 36, 38-42, Erikkson teach oral administration, solid dosage form (e.g. tablets), dosage regimen, dosage form suspended in vehicle and additional radiation therapy.
As to claims 43-45, it is noted that Veryaskina teach that myelodysplastic syndromes (MDS) is characterized by multilineage dysplasia, and chronic myelomonocytic leukemia is a subtype of MDS and MDS patients comprise four risk groups including low, high risks. A skilled artisan would have found it obvious and motivated to treat different types of MDS, or characterized by multilineage dysplasia or high risk MDS group(s) with tasquinimod to derive therapeutic benefits in MDS subjects.
As to claim 46, administration of an effective amount of tasquinimod to subjects with MDS from the teachings of the prior art will result in the improvement of one or more hematological parameters as claimed.
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 35-42, 46 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-17 of U.S. 12485095 (‘095).
The instant claims are directed to a method for the treatment of myelodysplastic syndrome (MDS) in a mammal in need of such treatment, by administration of a therapeutically effective amount of tasquinimod or a pharmaceutically acceptable salt thereof to the mammal. The dependent claims are limited to oral administration, solid dosage form, e.g. tablets, dosage amount (in the range of 0.001 mg to 0.2 mg/kg body weight), dosage amount, suspended in a vehicle, liquid, and further additional treatment, e.g. radiation.
‘095 reference claims are directed to plurality of particles comprising tasquinimod in free base form or as a pharmaceutically acceptable salt, a pharmaceutical composition and its use in a method of treating hematological cancer including myelodysplastic syndrome (claim 14). The dependent claims are limited to dosage unit of claim 7, containing the plurality of particles in an amount in the range of 0.2 mg to 1 mg, oral administration and dosage form includes tablet.
From the ‘095 reference claims, a person of ordinary skill in the art would have found it obvious to administer tasquinimod or its composition, oral administration e.g. as tablet (solid dosage form) in an amount of 0.7 mg for example (if 0.01 mg is administered to 70 kg subject) for treating myelodysplastic syndrome thus addressing claims 35-37, 39-40. As to claim 38, the dosage regimen is within the skill of an artisan (e.g. clinician) and is routinely optimized based on the condition, age etc. of the patient. As to claim 41, a person of ordinary skill in the art would have found it obvious to dissolve the solid dosage form e.g. tablet in liquid (water) for administration to patients who has difficulty in swallowing tablets. As to claim 42, it is well known in the art to provide radiation as additional therapy in the treatment of cancer, herein MDS. As to claim 46, administration of an effective amount of tasquinimod to subjects with MDS from the teachings of the prior art will result in the improvement of one or more hematological parameters as claimed.
Claims 43-45 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-17 of U.S. 12485095 (‘095) in view of Veryaskina et al. (Medicina 2020, 56, 376, p 1-16).
‘095 reference claims as above. The rejection is incorporated herein. The reference claims do not teach the limitations of claims 43-45.
Veryaskina et al. teachings discussed as above.
As to claims 43-45, Veryaskina teach that myelodysplastic syndromes (MDS) is characterized by multilineage dysplasia, and chronic myelomonocytic leukemia is a subtype of MDS and MDS patients comprise four risk groups including low, high risks. A skilled artisan would have found it obvious and motivated to treat different types of MDS, or characterized by multilineage dysplasia or high risk MDS group(s) with tasquinimod to derive therapeutic benefits in MDS subjects.
Claims 35-46 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-5, 7-15, 17-18 of US 10300053 (‘053) in view of Mondet (Molecules, 2021, 1323, p 1-16), Chen (Nature Medicine, 2019, 25, 103-110), and Veryaskina et al. (Medicina 2020, 56, 376, p 1-16).
The instant claims as above.
‘053 reference claims are directed to a method of treatment of leukemia selected from acute lymphoblastic leukemia and acute myeloid leukemia, by administering 4-hydroxy-5-methoxy-N,1-dimethyl-2-oxo-N-[4-(trifluoromethyl)phenyl]-1,2-dihydroquinoline-3-carboxamide (tasquinimod) or a pharmaceutically acceptable salt thereof to a mammal in need thereof. The dependent claims are limited to an amount of an amount of from 0.001 mg to 0.2 mg of the compound/kg of body weight per day, administration of the compound or salt 1-3 times a day, wherein the compound or salt is administered dissolved or suspended in a liquid vehicle, wherein the treatment further comprises radiation therapy and/or autologous stem cell transplantation, wherein the mammal is a human, wherein the treatment is by oral administration, a solid or semi-solid dosage form, capsule, a tablet or a pill.
The reference claims do not teach treating myelodysplastic syndrome with tasquinimod.
Mondet, Chen and Veryaskina as discussed above.
From the teachings of Mondet, Chen and Veryaskina a skilled artisan would have found it obvious that (i) changes in the expression levels of S100A8 and S100A9 proteins are observed both in acute myeloid leukemia and MDS (ii) tasquinimod targets the microenvironment by preventing interactions between TLR4, RAGE and S100A9 and (iii) myelodysplastic syndromes (MDS) progress to acute myeloid leukemia. The reference claim(s) is explicit in teaching the use of tasquinimod in AML. A person skilled in the art from the combined prior art teachings would have found it obvious to treat subjects with MDS with tasquinimod with a reasonable amount of success and derive therapeutic effects. As to the limitation of therapeutically effective amount, the reference claim 2 teach an amount ranging from 0.001 mg to 0.2 mg of the compound/kg of body weight per day of tasquinimod in treating AML. Thus a skilled artisan would have found it obvious to administer the same amount to treat MDS in subjects. Thus claims 35 and 37 are addressed.
As to claims 36, 38-42, the reference claims teach oral administration, solid dosage form (e.g. tablets), dosage regimen, dosage form suspended in vehicle and additional radiation therapy.
As to claims 43-45, it is noted that Veryaskina teach that myelodysplastic syndromes (MDS) is characterized by multilineage dysplasia, and chronic myelomonocytic leukemia is a subtype of MDS and MDS patients comprise four risk groups including low, high risks. A skilled artisan would have found it obvious and motivated to treat different types of MDS, or characterized by multilineage dysplasia or high risk MDS group(s) with tasquinimod to derive therapeutic benefits in MDS subjects.
As to claim 46, administration of an effective amount of tasquinimod to subjects with MDS from the teachings of the reference claims will result in the improvement of one or more hematological parameters as claimed.
Claims 35-42, 46 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of US 9956212 (‘212) or claims 1-12 of US 10314836 (‘836) in view of Namdaroğlu (Octa Oncologica Turcica, 2016, p 216-219).
The instant claims as above.
‘212 reference claims teach a method of treatment of multiple myeloma by administration to a mammal in need thereof of 4-hydroxy-5-methoxy-N,1-dimethyl-2-oxo-N-[4-(trifluoromethyl)phenyl]-1,2-dihydroquinoline-3-carboxamide (aka tasquinimod) (See claim 1). The dependent claims are limited to the treatment by oral administration, an amount ranging from 0.001 mg to 0.2 mg of the compound/kg of body weight per day, or of a corresponding amount of the pharmaceutically acceptable salt, by administration of the compound or salt 1-3 times a day, the compound is administered as solid dosage form, the solid dosage form is a tablet or capsule, the compound or salt is administered dissolved or suspended in a liquid vehicle, and the treatment further comprises radiation therapy and/or autologous stem cell transplantation.
‘836 reference claims are directed to method of treatment of multiple myeloma comprising administering an effective amount of the compound 4-hydroxy-5-methoxy-N,1-dimethyl-2-oxo-N-[4-(trifluoromethyl)phenyl]-1,2-dihydroquinoline-3-carboxamide (aka tasquinimod) or a pharmaceutically acceptable salt thereof to a human in need of such treatment. The dependent claims are limited to the treatment by oral administration, an amount ranging from 0.001 mg to 0.2 mg of the compound/kg of body weight per day, or of a corresponding amount of the pharmaceutically acceptable salt, by administration of the compound or salt 1-3 times a day, the compound is administered as solid dosage form, the solid dosage form is a tablet or capsule, the compound or salt is administered dissolved or suspended in a liquid vehicle, and the treatment further comprises radiation therapy and/or autologous stem cell transplantation.
The reference claims do not teach treating myelodysplastic syndrome with tasquinimod.
Namdaroğlu teaches a case report regarding the co-existence of multiple myeloma and myelodysplastic syndrome. There have been some reports of coexistence of MDS and myeloma; supporting the idea of pluripotent stem cell origin of the disease. We suggest that MM patients administrating with cytopenie should be evaluated for coexistent myeloid neoplasms (See Abstract, p 216).
A person skilled in the art from the teachings of the prior art would have found it obvious to administer tasquinimod in patients with MDS. From the combined teachings of the reference claims and Namdaroğlu a person of ordinary skill in the art would have found it obvious to administer a therapeutically effective amount of tasquinimod in treating MDS thus addressing claim 35. As to claims 36-42, one would have found it obvious to arrive at the limitations from the reference claims and the prior art. As to claim 46, administration of an effective amount of tasquinimod to subjects with MDS from the teachings of the reference claims will result in the improvement of one or more hematological parameters as claimed.
Claims 43-45 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of US 9956212 (‘212) or claims 1-18 of US 10314836 (‘836) in view of Namdaroğlu (Octa Oncologica Turcica, 2016, p 216-219) and further in view of Veryaskina et al. (Medicina 2020, 56, 376, p 1-16).
The reference claims as above. The rejection is incorporated herein. The reference claims and the prior art do not teach the limitations of claims 43-45.
Veryaskina et al. teachings discussed as above.
As to claims 43-45, Veryaskina teach that myelodysplastic syndromes (MDS) is characterized by multilineage dysplasia, and chronic myelomonocytic leukemia is a subtype of MDS and MDS patients comprise four risk groups including low, high risks. A skilled artisan would have found it obvious and motivated to treat different types of MDS, or characterized by multilineage dysplasia or high risk MDS group(s) with tasquinimod to derive therapeutic benefits in MDS subjects.
Claims 35-42, 46 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-7, 18, 21-25 of co-pending application, 17802124 (‘124, now allowed) in view of Namdaroğlu (Octa Oncologica Turcica, 2016, p 216-219) and Liberg et al. (US 9956212).
The instant claims as above.
‘124 reference claims are directed to a method of treatment of multiple myeloma in a subject, the method comprising administering to the subject tasquinimod, or a pharmaceutically acceptable salt thereof, in combination with at least one further compound selected from (i) a proteasome inhibitor,(ii) an immunomodulatory imide, and (iii) an antibody, wherein the proteasome inhibitor is selected from bortezomib and ixazomib; the immunomodulatory imide is lenalidomide; and the antibody is daratumumab. The dependent claims are limited to additional therapy and select additional agents.
The reference claims are not explicit in teaching treating MDS with tasquinimod or its amount.
Namdaroğlu teachings discussed as above.
Liberg et al. teach a method of treatment of multiple myeloma by administration to a mammal in need thereof of 4-hydroxy-5-methoxy-N,1-dimethyl-2-oxo-N-[4-(trifluoromethyl)phenyl]-1,2-dihydroquinoline-3-carboxamide (aka tasquinimod) (See claim 1). The dependent claims are limited to the treatment by oral administration, an amount ranging from 0.001 mg to 0.2 mg of the compound/kg of body weight per day, or of a corresponding amount of the pharmaceutically acceptable salt, by administration of the compound or salt 1-3 times a day, the compound is administered as solid dosage form, the solid dosage form is a tablet or capsule, the compound or salt is administered dissolved or suspended in a liquid vehicle, and the treatment further comprises radiation therapy and/or autologous stem cell transplantation (See claims 1-20).
A person skilled in the art from the teachings of the prior art would have found it obvious that MM and MDS coexist in patients and administer tasquinimod in patients with MDS for treatment. From the combined teachings of Namdaroğlu and Liberg a person of ordinary skill in the art would have found it obvious to administer a therapeutically effective amount of tasquinimod in treating MDS thus addressing claim 35. As to claims 36-42, one would have found it obvious to arrive at the limitations from the prior art Liberg’s teachings. As to claim 46, administration of an effective amount of tasquinimod to subjects with MDS from the teachings of the reference claims will result in the improvement of one or more hematological parameters as claimed.
Claims 43-45 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-7, 18, 21-25 of co-pending application, 17/802124 (‘124, now allowed) in view of Namdaroğlu (Octa Oncologica Turcica, 2016, p 216-219) and Liberg et al. (US 9956212) and further in view of Veryaskina et al. (Medicina 2020, 56, 376, p 1-16).
The reference claims as above. The rejection is incorporated herein. The reference claims and the prior art do not teach the limitations of claims 43-45.
Veryaskina et al. teachings discussed as above.
As to claims 43-45, Veryaskina teach that myelodysplastic syndromes (MDS) is characterized by multilineage dysplasia, and chronic myelomonocytic leukemia is a subtype of MDS and MDS patients comprise four risk groups including low, high risks. A skilled artisan would have found it obvious and motivated to treat different types of MDS, or characterized by multilineage dysplasia or high risk MDS group(s) with tasquinimod to derive therapeutic benefits in MDS subjects.
This is a provisional nonstatutory double patenting rejection.
Claims 35-42, 46 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-7, 21-23 of co-pending application 18/571472 (‘472) in view of Liberg et al. (US 9956212).
The instant claims as above.
‘472 reference claims are directed to a pharmaceutical composition comprising a therapeutically effective amount of tasquinimod and its use in treating hematological cancer including myelodysplastic syndrome and multiple myeloma.
The reference claims are not explicit in teaching the amount of tasquinimod in the method.
Liberg as discussed above.
From Liberg a person of ordinary skill in the art would have found it obvious that an effective amount of tasquinimod can range from 0.001 mg to 0.2 mg of the compound/kg of body weight per day for the treatment of multiple myeloma. Hence a skilled artisan would have found it obvious the same amount in treating MDS. Thus claims 35 and 37 would have been obvious over the reference claims and Liberg. As to claims 36, 38-42, one would have found it obvious to arrive at the limitations from the prior art Liberg’s teachings. As to claim 46, administration of an effective amount of tasquinimod to subjects with MDS from the teachings of the reference claims will result in the improvement of one or more hematological parameters as claimed.
Claims 43-45 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-7, 21-23 of co-pending application 18571472 (‘472) in view of Liberg et al. (US 9956212) and further in view of Veryaskina et al. (Medicina 2020, 56, 376, p 1-16).
The reference claims as above. The rejection is incorporated herein. The reference claims and the prior art do not teach the limitations of claims 43-45.
Veryaskina et al. teachings discussed as above.
As to claims 43-45, Veryaskina teach that myelodysplastic syndromes (MDS) is characterized by multilineage dysplasia, and chronic myelomonocytic leukemia is a subtype of MDS and MDS patients comprise four risk groups including low, high risks. A skilled artisan would have found it obvious and motivated to treat different types of MDS, or characterized by multilineage dysplasia or high risk MDS group(s) with tasquinimod to derive therapeutic benefits in MDS subjects.
This is a provisional nonstatutory double patenting rejection.
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to UMAMAHESWARI RAMACHANDRAN whose telephone number is (571)272-9926. The examiner can normally be reached M-F- 8:30-5:00 PM (PST).
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Kortney Klinkel can be reached at 5712705239. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/ docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/Umamaheswari Ramachandran/Primary Examiner, Art Unit 1627