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 .
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.
Claims 13-20 and 29-37 are rejected under 35 U.S.C. 103 as being unpatentable over Noguchi et al. (US Patent No. 20210085667) in view of Ying et al. Over-expression of P2X7 receptors in spinal glial cells contributes to the development of chronic postsurgical pain induced by skin/muscle incision and retraction (SMIR) in rats, Experimental Neurology, September 2014, Pages 836-843 and Ursu et al. Gain and loss of function of P2X, receptors: mechanisms, pharmacology and relevance to diabetic neuropathic pain, Molecular Pain, 2014, Pages 1-11.
Regarding claims 13, 16, 18-20, 29-31 and 35-37, Noguchi teaches a method for the treatment for neuropathic pain of peripheral neuropathy and diabetic neuropathy (relevant to claims 13 and 16) (para. 0645) comprising P2X7 receptor antagonist of (5S,8S)-N-(2,4-dichloro benzyl)-5-fluoro-8- hydroxy-8- (hydroxymethyl)-5,6,7,8- tetrahydroquinoline-5- carboxamide, (5S,8S)-N-(2-chloro-4- fluorobenzyl)-5- fluoro-8-hydroxy-8- (hydroxymethyl)-5,6,7,8- tetrahydroquinoline-5- carboxamide, (5S,8S)-N-(2,4-dichloro- 6-fluorobenzyl)-5- fluoro-8-hydroxy-8- (hydroxymethyl)-5,6,7,8- tetrahydroquinoline-5- carboxamide, (5S,8S)-N-(2-chloro-4,6- difluorobenzyl)-5- fluoro-8-hydroxy-8- (hydroxymethyl)-5,6,7,8- tetrahydroquinoline-5- carboxamide (relevant to claims 18-20 and 29-31 and 35-37) (Table 54).
Noguchi fails to teach the treatment of P2X7 receptor neuropathic pain as postoperative pain and P2X7 receptor gain of function.
Ying teaches P2X7 receptor antagonist of BBG and A438079 prevent skin/muscle incision retraction (SMIR) induced mechanical allodynia which is a neuropathic pain (page 839, right column, fig. 7). Ying additionally teaches the mechanism of postsurgical pain is directly related to the upregulation of the P2X7 receptor by SMIR (relevant to claims 32-34) (abstract).
Ursu teaches single nucleotide polymorphisms (SNPs) in the gene P2RX7, coding for the ATP-gated ion channel P2X7, have been described that of cause gain-of-function (GOF) and loss-of-function (LOF). P2RX7 SNPs have been associated with more or less severe pain scores in patient suffering of post-mastectomy pain and osteoarthritis (abstract). Ursu additionally teaches the study of P2RX7 SNPs rs208294, rs1718119 and rs3751143 transfection in НЕK-293 cells caused gain- and loss-of function phenotypes. In addition P2X7 receptor antagonist of A-804598, A740003 and AZ11654373 blocked either channel or pore activity in the three P2X7 variants while showing no significant result difference between the antagonist, showing that despite the difference in P2X7 variants, their function and mechanism of being blocked are similar (relevant to claims 14-15)(page 4, right column to page 5 left column).
Therefore, It would have been obvious to someone of ordinary skill in the art at the time of filling to have used the P2X7 receptor antagonist taught by Noguchi to treat postoperative pain and P2X7 receptor gain of function. One would have been motivated to do so from the teachings of Ying on P2X7 receptor antagonist are known for treatment of postoperative pain and Ursu on the use of P2X7 receptor antagonist having the same effect on P2X7 receptor gain of function variants. There is a reasonable expectation of having the same outcome of treatment on P2X7 receptor postoperative pain and P2X7 receptor gain of function as the P2X7 receptor antagonist taught by Ying and Ursu as the P2X7 receptor antagonist taught by Noguchi.
Conclusion
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MIKHAIL O'DONNEL. ROBINSON
Examiner
Art Unit 1627
/MIKHAIL O'DONNEL ROBINSON/Examiner, Art Unit 1627
/SARAH PIHONAK/Primary Examiner, Art Unit 1627