DETAILED ACTION
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 .
Status of the Application
This Office Action is in response to applicant’s arguments filed on 1/20/26. Claims 2-11 have been cancelled. Claims 13-18 have been added. Claims 1, 12-18 are pending. Claim 1 has been amended. Claims 1, 12-18 are examined herein.
The cancellation of claim 3 has rendered the 102(a)(1) rejection over Chen et al. moot, therefore hereby withdrawn.
Applicant’s arguments with respect to the 102(a)(1) rejection over Zuo et al. has been fully considered but found not persuasive, therefore maintained for reasons of record and modified below due to the claim amendments.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale or otherwise available to the public before the effective filing date of the claimed invention.
Claims 1, 12-18 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Zuo et al. (WO 2018/204226 A1, of record).
Zuo et al. teach a method for the treatment or prevention of hearing loss by administering to an animal in need thereof an inhibitor of epidermal growth factor receptor (EGFR) signaling (paragraph 0005). Preferred EGFR inhibitors are afatinib and AZD3759 (paragraphs 0032, 0054, 00151). Hearing loss may be from damage caused by cisplatin, antibiotics, noise, aging, ototoxic insults, medicines, such as antibiotics, and some cancer treatments, for example chemotherapy and radiation therapy (paragraphs 0010, 0064, 0069, 0072). Hearing impairment may also be drug-induced, such as from the chemotherapeutic agent, cisplatin (paragraph 0073). In various aspects, the disclosed molecules can be used in combination with one or more other drugs in the treatment, prevention, control, amelioration, or reduction of risk of hearing impairments and disorders for which disclosed molecules or the other drugs can have utility, where the combination of the drugs together are safer or more effective than either drug alone. Figure 4 shows that a EGFR inhibitor protects against cisplatin induced hair cell loss (paragraph 0009). Kits may include active agents as well as instructions for use (paragraph 00138). The dose of the drug should be sufficient to affect the desired response over a reasonable time frame. One skilled in the art will recognize that dosage will depend upon a variety of factors, including age, species, location of damaged sensory epithelia, the pathology, and condition or disease state. Dosage also depends on the EGFR inhibitor, the route, timing, and frequency of administration, as well as the existence, nature, and extent of any side effects (paragraph 00129).
It is noted that the limitations drawn to “protects a plurality of outer and inner hair cells” are inherent since it will necessarily occur when the same active agent is administered to the same patient population.
Response to Arguments
Applicant argues that claim 1 calls for “orally administering” afatinib “to the subject prior to noise exposure.” These limitations are not present in St. Jude. Furthermore, Applicant argues that St. Jude discloses hundreds of EGFR compounds including afatinib, which according to Example 4 is associated with protection against cisplatin-induced hair cell loss and not damage from noise exposure. Most of the 75 kinase inhibitors that were screened did not show the potential ability to protect against cisplatin induced hair loss.
This is not persuasive because Zuo et al. clearly teach a method for the treatment or prevention of hearing loss by administering to an animal in need thereof an inhibitor of epidermal growth factor receptor (EGFR) signaling (paragraph 0005). Preferred EGFR inhibitors are afatinib and AZD3759 (paragraphs 0032, 0054, 00151). Hearing loss may be from damage caused by cisplatin, antibiotics, noise, aging, ototoxic insults, medicines, such as antibiotics, and some cancer treatments, for example chemotherapy and radiation therapy (paragraphs 0010, 0064, 0069, 0072). Therefore, it is clear that the authors view afatinib as a preferred EGFR inhibitor. Moreover, the fact that Example 4 may be drawn to damage not associated with noise exposure matters little since the broad teaching encompasses this limitation.
It is well-settled that disclosed examples and preferred embodiments do not constitute a teaching away from a broader disclosure or nonpreferred embodiments. In re Susi, 440 F.2d 442, 169 USPQ 423 (CCPA 1971). "A known or obvious composition does not become patentable simply because it has been described as somewhat inferior to some other product for the same use." In re Gurley, 27 F.3d 551, 554, 31, USPQ2d 1130, 1132 (Fed. Cir. 1994).
Applicant argues that the language in the cited prior art with respect to protection of mammalian ear cells from damage caused by noise exposure is speculative at best.
This is not persuasive because every limitation in the claims have been taught by the cited prior art, therefore no speculation is needed.
Applicant points to the declaration filed on 5/12/25, which provides data to show that cisplatin and noise induced hearing loss are vastly different diseases, which require vastly different therapeutic drugs.
This is not persuasive because Applicant is reminded that the rejection of record is a 102 anticipatory rejection and not a 103 obviousness rejection. Therefore, a showing of secondary consideration, for example evidence presented in a declaration, is insufficient to overcome a 102 anticipatory rejection.
Applicant also argues that the particular result of “prevent ear cell loss caused by noise exposure” is not shown in the cited art. Applicant argues that the Chen review article notes that different drugs are efficacious on different types of hearing loss. The present application provides in vivo data in an animal model and data from mice. Claim 1 requires a particular result that is not shown in the cited art. St. Jude does not enable one of ordinary skill in the art to practice the claimed invention. This is because one skilled in the art would know that EGFR inhibitors can induce ototoxicity as taught by Aylin et al.
This is not persuasive because since the same claimed active agent (afatinib) is being administered to the same claimed patient population (anyone that is need of prevention of hearing loss), it is inherent that prevention of hearing loss will necessarily occur. Regardless, Applicant is reminded that the prior art need not teach enablement of every embodiment as long as there is sufficient teaching of every limitation of the claims. Finally, the arguments directed to unpredictability in the art or no reasonable expectation of success is irrelevant because the rejection of record is not a 103 obviousness rejection, but a 102 anticipatory rejection.
Applicant argues that it is known that EGFR inhibitors that are used in medical treatments have a side effect of loss of hearing and tinnitus as shown in Alexeeva et al. Thus, one skill in the art cannot reasonably infer from the prior art that afatinib is effective to prevent ear cell loss caused by noise.
This is not persuasive because the Alexeeva reference was not used in the making the prior art rejection, nor is the Alexeeva reference sufficient to establish the state of the art. Furthermore, the teachings of Alexeeva refer to medical treatment that have nothing to do with treating hearing loss.
Applicant also argues that certain EGFR inhibitors that are used in medical treatments have a known side effect of loss of hearing and tinnitus, such as axitinib and ruxolitinib, as shown by Alexeeva. Therefore, one skilled in the art cannot reasonably infer that afatinib is effective in preventing ear cell loss caused by noise.
This is not persuasive because no where in Alexeeva does it mention afatinib, therefore no conclusions can be made regarding not preventing ear cell loss.
Conclusion
THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any extension fee pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Yong S. Chong whose telephone number is (571)-272-8513. The examiner can normally be reached Monday to Friday: 9 AM to 5 PM EST.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Adam Milligan, can be reached at (571)-270-7674. The fax phone number for the organization where this application or proceeding is assigned is (571)-273-8300.
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/Yong S. Chong/Primary Examiner, Art Unit 1623
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