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 .
Application Status
Claims 1, 7, 9-10, 26-29, 31, 40-43, 48, and 52-56 are currently pending.
Priority
This application claims priority to US Provisional Application 63/220,400, filed on 7/9/2021.
Claim Objection
Claim 1 is objected to because of the following informalities: applicant recites a “sense strand having the structure (NAG37s-(invAb)sguggacuuCIUfCfucaauuuucus(inv Ab) or SEQ ID NO: 11. Looking towards the specification for guidance, the bolded modification for SEQ ID NO: 11 is listed as CfUfCf, not CIUfCf (see Table 3). Furthermore, Table 5 provides a list of abbreviations for the modifications wherein Cf is a 2’-fluorocytidine-3’-phoshate modification, however, there is no modification listed for CI.
Claim 26 and 27 are objected to because of the following informalities: claims 26 and 27 recites “RNAi component is adminsteredto the subject”. Here, a space is needed between ‘administered’ and ‘to’.
Claim 29 is objected to because of the following informalities: claim 29 recites “RNAi component is administeredvia” where a space is needed between ‘administered’ and ‘via’.
Claim 53 is objected to because the figure depicting the sodium salt having the following structure is unclear as the resolution of the image is too low to determine essential features. Examiner will interpret the claimed structure with guidance from the instant specification, wherein the structure is disclosed on paragraph 0100-0106.
Appropriate correction is required.
Claim Interpretation
In view of the foregoing, Claim 1 will be examined as if the modification is CfUfCf, absent evidence to the contrary.
Claim Rejection 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claim 27 is rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Regarding claim 27, the phrase "for example" or in this case, (i.e.) renders the claim indefinite because it is unclear whether the limitation(s) following the phrase are part of the claimed invention. See MPEP § 2173.05(d).
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.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 1, 26, 27, 29, 31, 40-43, 48, and 52-53 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Li et al. (US 2019/0255091 A1) as evidenced by Deray et al. (Hepatitis B Virus Infection and the Kidney: Renal Abnormalities in HBV Patients, Antiviral Drugs Handling, and Specific Follow Up, Advances in Hepatology, Volume 2015, Article ID 596829, all pages, 2/28/2015).
Regarding claim 1, Li teaches compositions and methods for inhibition of Hepatitis B virus gene expression with RNA interference (see abstract), wherein the composition comprises RNAi agents that include at least a sense strand and an antisense strand, wherein the sense and antisense strand can be partially, substantially, or fully complementary to each other (see paragraph 0014). Li teaches, in some embodiments, an HBV RNAi agent disclosed herein consists of or comprises AD05070 linked to NAG37s (see paragraph 0314).
Regarding the SEQ ID pairs recited in the instant application (SEQ ID NO: 2 and 11, and 8 and 16), Li teaches SEQ ID NO: 126, 253, 140, and 262, which has 100% identity to the sequence and modifications claimed in SEQ ID NO: 2 and 11, and 8 and 16, respectively (see Table 4).
Regarding the first and second RNAi agents being linked to NAG37s, Li teaches claim 114 which recites “wherein a combination of at least two RNAi agents comprising a first RNAi agent and a second RNAi agent, wherein:… “ followed by claim 117 which ultimately depends on claim 114, which recites “wherein the targeting ligand is selected from the group consisting of … (NAG37)”, indicating that both RNAi agents can be linked to NAG37s.
Regarding the structure of NAG37(s), Li teaches HBV RNAi linked to NAG37s shown as a sodium salt having the structure disclosed in paragraph 0314. Here, the structure of NAG37s is 100% identical to the structure of NAG37s recited in the instant claim. Furthermore, Li teaches modifications where a, g, c, u are 2’-O-methyl modifications (see paragraph 0387, 0389, 0391, and 0395), Af, Cf, Gf, and Uf are 2’-flouro modified nucleotides (see paragraph 0398, 0400, 0402, 0406), s is a phosphorothioate internucleoside linkage (see paragraph 0423) and invAb is an inverted abasic deoxyribonucleotide (see paragraph 0420).
Regarding the molar ratio of the first RNAi agent to the second, Li teaches in paragraph 0307 where the ratio of AD04872 to AD05070 is about 2:1. Furthermore, claim 83 and 84 of Li recites “wherein the ratio of the one or more RNAi agents to the additional RNAi agent by weight is in the range of about 1:2 (claim 83) or 2:1 (claim 84).
Regarding claim 26, Li teaches where an effective amount of an active compound will be in the range from 0.1 to about 100 mg/kg of bodyweight/day (see paragraph 0480). The instant claim recites where the RNAi component is administered to the subject in a dose of about 40 to 200 mg. It would be obvious that a patient with a hypothetical weight of 125 lbs (or 56kg) could be administered a dose of 1mg per kg, as recited in Li, to reach a dosage amount of 56 mg. Though this is a merely an example, the range claimed in the instant application could be arrived at by applying the dosage range provided in Li.
Regarding claim 27, Li teaches Table 47, which discloses dosing regiments for HBV-infected FRG humanized model mice, wherein each mouse was given a subcutaneous administration of the HBV RNAi agent(s) on day 1 and on day 29, if still alive on day 29 (see paragraph 0600). Here, the instant claim 27 provides an example where once monthly can be every four weeks (i.e. Q4W). As four weeks represents a period of 28 days, administering a dosage on day one and on day 29 qualifies as administering an RNAi agent in a monthly interval.
Regarding claim 29, Li teaches in some embodiments, the described HBV RNAi agent(s) may be administered to a subject in need thereof via subcutaneous injection (see paragraph 0324).
Regarding claim 31, Li teaches in some embodiments, the described HBV RNAI agent(s) are optionally combined with one or more additional (i.e., second, third, etc.) therapeutics. A second therapeutic can be another HBV RNAi agent (see paragraph 0322).
Regarding claim 40-43, Li teaches in some embodiments, the described RNAi agent(s) are optionally combined with one or more additional therapeutics, wherein the additional therapeutic is a nucleoside inhibitor or nucleotide inhibitor (see paragraph 0323). Said RNAi agent(s) are optionally combined with entecavir, tenoforvir, tenoforvir alafenamide, tenoforvir disoproxil, lamivudine, etc. (see paragraph 0323).
Regarding claim 48, Li teaches example 18 (paragraph 0597) that discloses a treatment example of HBV RNAi agents in an HBV-infected humanized mouse model. Here, mice were administered an oral daily gavage with entecavir to inhibit HBV replication. Daily dosing of entecavir continued until the day mice were euthanized. Entecavir administration was expected to reduce serum HBV DNA in chronically infected human patients, but not reduce HBsAg (see paragraph 0598). The conclusion of this example was that administration of entecavir reduced viral replication in both the absence and presence of HBV RNAi agents (see paragraph 0603). Therefore, Li administers an RNAi agent once, on day one (see Table 47), but continues to administer entecavir until euthanizing the mice.
Regarding claim 52 and 53, Li teaches where an HBV RNAi agent disclosed herein comprises AD05070 linked to NAG37s, shown as a sodium salt with a disclosed structure (see paragraph 0314). The disclosed structure of claim 53 has 100% identity to the structure disclosed in paragraph 0314.
Though Li does not disclose wherein the patient has been previously determined to have mild renal impairment, Deray teaches that chronic HBV infection has been linked to renal disease for decades, wherein renal injury caused by HBV may be related to immune reactions (see section 2.1 of Deray). Deray teaches that the prevalence of an abnormal GFR at baseline was determined in two cohorts of 145 CHB patients planned to receive a treatment or placebo. In the study, the prevalence of a “mildly impaired” GFR did not differ between the two groups. This results emphasizes that impaired renal function is highly prevalent in CHB patients, independently of any treatment with a potential nephrotoxicity (see section 2.3 of Deray). As Li teaches compositions and methods of treating patients with chronic HBV, patients who suffer from chronic HBV will also have mild renal impairment, evidenced by Deray.
In view of the foregoing, claims 1, 26, 27, 29, 31, 40-43, 48, and 52-53 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Li.
Claims 28 and 54-56 are rejected under 35 U.S.C. 103 as being unpatentable over Deray et al. (Hepatitis B Virus Infection and the Kidney: Renal Abnormalities in HBV Patients, Antiviral Drugs Handling, and Specific Follow Up, Advances in Hepatology, Volume 2015, Article ID 596829, all pages, 2/28/2015) in view of Li et al. (US 2019/0255091 A1, published 8/22/2019), Chen et al. (RNAi for Treating Hepatitis B Viral Infection, SPRINGER NATURE, Volume 25, pgs. 72-86, published 12/12/2007), and Wooddell et al. (RNAi-Based Treatment of Chronically Infected Patients and Chimpanzees Implicates Integrated Hepatitis B Virus DNA as a Source of HBsAg, Sci Transl Med., Volume 9, Issue 409, all pages, published 3/27/2018).
Regarding the method of treating chronic hepatitis B virus comprising administering to a subject, with a mild renal impairment, an effective amount of a pharmaceutical composition that comprises an RNAi component recited in the claims above, the compositions and methods are taught in the combined arts of Deray and Li.
Regarding claims 54-55, Li teaches where the ratio of AD04872 to AD05070 is about 2:1 (see paragraph 0307) and where in some embodiments, about 2.0mg/kg of AD04872 (RNAi agent 1) and about 1.0mg/kg AD05070 (RNAi agent 2) are administered to a subject in need thereof (see paragraph 0308).
The combined arts of Deray and Li does not teach wherein the RNAi component is administered to a subject for 12 to 48 weeks (claim 28) or at least 20 weeks (claim 56), or where the first and second RNAi agent are administered in an amount of about 33mg and 17 mg, respectively (claim 54) or 133mg and 67mg, respectively (claim 55).
Regarding claim 28 and 56, Chen teaches RNAi for treating hepatitis B viral infection. Chen discloses that while RNAi can inhibit HBV gene expression and replication, and it might have the potential to revolutionize the treatment of HBV, the level of HBV gene silencing greatly depends on siRNA sequences and dose (see concluding remarks). When treated with only nucleoside analogues alone, in patients who did not lose HBeAg (the protein indicative of HBV infection), stopping therapy after 3 to 12 months is usually followed up by a return of HBV DNA to pretreatment values and relapse of disease (see section titled combination of siRNA and nucleoside analogues). Furthermore, Chen discloses where the combination of siRNA and lamivudine (a nucleoside analogue) may exhibit greater inhibitory effect on HBV replication.
Regarding claims 28 and 56, Wooddell teaches where chimps who are HBeAg + and – were treated with daily oral NUCs for 8-24 weeks to reduce viral replication prior to dosing with ARC-520. While continuing NUC treatment, the chimpanzees were then given ARC-520 once every 4 weeks, for a total of 6 to 11 injections (approximately 6 to 12 months) (see Fig. 2 of Wooddell). In a human clinical study involving intravenous doses of ARC-520 administered in varying concentrations, modest decreases in HBsAg levels were seen in cohorts with lower time periods on NUCs. HBsAg levels decrease most sharply during the first 8 days after dosing in all cohorts, reaching a plateau before starting to relapse 6-8 weeks after dosing (see results section).
It would have been obvious to one with ordinary skill in the art, before the effective filing date of the claimed invention, to combine the teachings of Deray, Li, Chen, and Wooddell, to arrive at the instantly claimed invention.
One would expect a reasonable chance of success as Li, Chen, and Wooddell all disclose RNAi as a method for treating CHB in a patient or subject. Regarding claims 54 and 55, though the exact dosage is not recited in the listed arts above, the ratio of one RNAi agent to another is approximately 2:1, which is a ratio disclosed in Li. Furthermore, Li directs dosage as 2.0 mg/kg of a first RNAi agent and 1.0 mg/kg of a second RNAi agent (see paragraph 0308 of Li). In the instant application, a 33 mg and 17 mg dosage would approximate to a 17kg subject (claim 54) and a 133 mg and 67 mg dose would approximate to a 67kg subject. Looking to the instant specification for guidance, applicant discloses a “subject” can refer to a human or non-human primate, wherein a non-human primate would fall under a reasonable weight of 17 kg and a human would fall under a reasonable weight of 67 kg, absent evidence to the contrary. Furthermore, under MPEP 2144.05, in the event of overlapping, approaching, and similar ranges, amounts, and proportions, a prima facie case of obviousness exists. Furthermore, MPEP 2144.05 section II discloses differences in concentration or temperature will not support the patentability of subject matter encompassed by the prior art unless there is evidence indicating such concentration and temperature is critical. Though the dosage taught by Li can be interpreted to fall within the range claimed in the instant application, one would arrive at the dosage limitations of claim 54 and 55 simply through routine optimization of dosing a subject at a 2:1 RNAi agent ratio based off weight, as disclosed in Li.
One would be motivated to do so as Chen discloses that the level of HBV gene silencing greatly depends on siRNA sequences and dose (see conclusion of Chen). This is greater exemplified in the experiments of Wooddell, where patients in different cohorts administered with different dosages displayed different levels of reduction in HBsAg levels associated with CHB. Seemingly so, cohorts administered with higher dosages or multiple dosages exhibited great initial HBsAg reduction in the initial 8 week timeframe (see Fig. 1 of Wooddell). Furthermore, regarding claims 28 and 56, Chen teaches that in patients treated with nucleoside analogues, those who did not lose HBeAg and stopped treatment after 3 to 12 months, showed a return of HBV DNA to pretreatment levels and relapse of disease (see section titled ‘Combination of siRNA and Nucleoside Analogues’). Though Chen does not mention siRNA treatment in terms of time frame, only that combination of siRNA and NUCs could exhibit a greater inhibitory effect on HBV replication, Wooddell showed this experimentally where in all human cohorts that were administered a single dose or multiple doses of RNAi within a starting time period exhibited relapse 6-8 weeks after dosing (see Fig. 1). In a chimpanzee study with repeat dosing from 6 to 12 months, levels of HBsAg reduction was greater in all subjects through longer time periods of continued treatment (see Fig. 2).
Therefore, it is clear, based off the teachings of Chen and Wooddell, that a key component of treating CHB in a subject is proper dosage of RNAi as well as treatment timeframe and it would be obvious to one skilled in the art to design and optimize a method of treatment to consider these factors.
In view of the foregoing, claims 28 and 54-56 are rejected under 35 U.S.C. 103 as being prima facie obvious, before the effective filing date.
Claims 9 and 10 are rejected under 35 U.S.C. 103 as being unpatentable over Deray et al. (Hepatitis B Virus Infection and the Kidney: Renal Abnormalities in HBV Patients, Antiviral Drugs Handling, and Specific Follow Up, Advances in Hepatology, Volume 2015, Article ID 596829, all pages, 2/28/2015) in view of Li et al. (US 2019/0255091 A1, published 8/22/2019), and Wooddell et al. (RNAi-Based Treatment of Chronically Infected Patients and Chimpanzees Implicates Integrated Hepatitis B Virus DNA as a Source of HBsAg, Sci Transl Med., Volume 9, Issue 409, all pages, published 3/27/2018).
Regarding the method of treating chronic hepatitis B virus comprising administering to a subject, with a mild renal impairment, an effective amount of a pharmaceutical composition that comprises an RNAi component recited in the claims above, the compositions and methods are taught in the combined arts of Deray and Li.
The combined arts of Deray and Li does not teach where the subject is a treatment naïve patient and where the subject is treatment naïve HBeAg+.
Regarding claims 9 and 10, Wooddell teaches where in a human clinical trial with ARC-250, a RNAi-based therapeutic targeting HBV transcripts, HBV S antigen (HBsAg) was strongly reduced in treatment-naïve patients positive for HBV e antigen (HBeAg+) but was reduced significantly less in patients that were HBeAg negative or had received long-term therapy with nucleoside viral replication inhibitors (NUCs) (see abstract). Wooddell teaches HBeAg and HBsAg play important roles in chronic infection. HBeAg is thought to induce T cell tolerance and allow viral persistence while HBsAg, in high levels, are believed to contribute to T-cell exhaustion, resulting in limited or weak T-cell responses (see introduction). For CHB patients, the desired endpoint of treatment is seroclearance of HBsAg, referred to as “functional cure” resulting in improved long-term prognosis. HBsAg loss is considered a hallmark of effective immune control of HBV (see introduction). Wooddell teaches initial RNAi agents were designed to target transcripts produced by cccDNA, where HBsAg is primarily produced by integrated HBV DNA rather than episomal cccDNA. Wooddell showed that liver HBV DNA was present at lower levels in HBeAg negative chimpanzees compared to HBeAg positive chimpanzees, and the level of HBV DNA was largely unchanged by NUCs. This suggest that the majority of HBV DNA in the HBeAg negative chimpanzees was not dependent on active HBV replication, but rather HBV DNA already integrated into the host chromosome (see discussion), which is not targetable by RNAi targeting cccDNA. As a result, individuals who are HBeAg positive means the vast majority of circulating viral proteins, including HBsAg, in this phase are produced by the transcriptionally active cccDNA in the liver, which RNAi directly silences (see discussion).
It would have been obvious to one with ordinary skill in the art, before the effective filing date of the claimed invention, to combine the teachings of Deray, Li, and Wooddell, to arrive at the instantly claimed invention.
One would have been motivated to apply the method of treating CHB with RNAi, as disclosed in Li, to a subject that is HBeAg+ treatment naïve to achieve greater efficacy of RNAi treatment. This is because Wooddell teaches that patients who are HBeAg+ and treatment naïve responded better to RNAi agents compared to those who were HBeAg+ negative or have undergone long-term NUC treatment (see results section). Versions of RNAi, such as ARC-520, targets transcripts generated by cccDNA (see introduction). Once a patient is HBeAg- due to chronic disease progression or has undergone NUC treatment, HBV DNA incorporated into host’s genome takes over the production of HBsAg as opposed to cccDNA (see discussion), making them un-targetable by certain RNAi therapies and explains why HBeAg- patients showed a lower magnitude of HBsAg reduction. Therefore, subjects who are HBeAg+ and treatment naïve represent an ideal candidate for RNAi treatment of CHB.
In view of the foregoing, claims 9 and 10 are rejected under 35 U.S.C. 103 as being prima facie obvious, before the effective filing date.
Claim 7 is rejected under 35 U.S.C. 103 as being unpatentable over Deray et al. (Hepatitis B Virus Infection and the Kidney: Renal Abnormalities in HBV Patients, Antiviral Drugs Handling, and Specific Follow Up, Advances in Hepatology, Volume 2015, Article ID 596829, all pages, 2/28/2015) in view of Li et al. (US 2019/0255091 A1, published 8/22/2019) and Severity Grading In Drug Induced Liver Injury (LiverTox®: Clinical and Research Information on Drug-Induced Liver Injury [Internet]. Bethesda (MD)L National Institute of Diabetes and Digestive and Kidney Diseases; 2012-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK548241/, last updated 5/4/2019), herein referred to as ‘LiverTox’, and Rogers et al. (Management of Acute Pancreatitis Associated with Checkpoint Inhibitors, J Adv Pract Oncol, Volume 11, Issue 1, published 1/1/2020).
Regarding the method of treating chronic hepatitis B virus comprising administering to a subject, with a mild renal impairment, an effective amount of a pharmaceutical composition that comprises an RNAi component recited in the claims above, the compositions and methods are taught in the combined arts of Deray and Li.
Regarding claim 7, Deray and Li does not teach wherein the subject has an ALT/AST<2 ULN, a direct bilirubin < 1.1 ULN, and a lipase level < Grade 2.
Regarding claim 7, LiverTox teaches the severity of cases of drug induced liver injury can vary greatly, from mild, transient, and asymptomatic elevations in serum enzyme levels to acute liver failure. LiverTox teaches a 5 point scale for grading the severity of liver injury based upon the presence of jaundice, hospitalization, signs of hepatic or other organ failure, and ultimate outcome. In the prospective clinical trials of medications, standard criteria are used to assess the severity of adverse events including symptoms and laboratory test abnormalities. Adverse events are typically graded on a scale of 0 to 4. Grades for severity of liver test abnormalities and symptoms of liver injury have been developed and standardized and are used in many publications of clinical trials and studies of new medications. In this system, the following levels are used to assess severity, with the values expressed as multiples of the upper limit of the normal range (ULN). Shown below is the provided grade scale.
PNG
media_image1.png
197
500
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Greyscale
Regarding claim 7, Rogers teaches that an estimated 0.1% to 2% of acute pancreatitis is associated with drugs (see section titled ‘Case Study’) and Table 2, shown below, which indicates Lipase grade levels with regards to pancreatitis. According to Table 2, a lipase level under grade 2 indicates a normal, healthy subject, that is not experiencing symptoms associated with pancreatitis.
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media_image2.png
789
768
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Greyscale
It would have been obvious to one with ordinary skill in the art, before the effective filing date of the claimed invention, to combine the teachings of Deray, Li, LiverTox, and Rogers, to arrive at the claimed invention, wherein the subject has an ALT/AST <2 ULN, a direct bilirubin < 1.1 ULN, and a lipase level < grade 2.
One would have been motivated to do so as the teachings of LiverTox shows ALT/AST < 2 ULN and bilirubin < 1.1 ULN is representative of healthy liver conditions and serum enzyme levels with regards to drug administration. Rogers shows that a lipase level < grade 2 represents a normal level of pancreatic enzyme, wherein a higher grade could represent pancreatitis. Both LiverTox and Rogers disclose that the use of drugs, in the case of clinical trials, could result in elevated serum enzyme levels seen in liver injury as well as pancreatitis. By administering a drug, such as an RNAi therapy taught by Li, to patients that exhibit abnormal liver enzyme levels or signs of acute pancreatitis could further cause unnecessary damage. Therefore, it would be obvious that for the administration of a pharmaceutical composition comprising RNAi, it would be imperative to do so to administer it to a subject that does not exhibit abnormal liver or pancreas conditions. ALT/AST < 2 ULN, bilirubin < 1.1 ULN, and a lipase level < grade 2 represents a subject that is healthy (with regards to liver and pancreas levels) and could represent a candidate for RNAi based drugs. This is evident in a prophetic example of a study provided by the applicant wherein both healthy and
In view of the foregoing, claim 7 is rejected under 35 U.S.C. 103 as being prima facie obvious before the effective filing date.
Double Patenting
A rejection based on double patenting of the “same invention” type finds its support in the language of 35 U.S.C. 101 which states that “whoever invents or discovers any new and useful process... may obtain a patent therefor...” (Emphasis added). Thus, the term “same invention,” in this context, means an invention drawn to identical subject matter. See Miller v. Eagle Mfg. Co., 151 U.S. 186 (1894); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Ockert, 245 F.2d 467, 114 USPQ 330 (CCPA 1957).
A statutory type (35 U.S.C. 101) double patenting rejection can be overcome by canceling or amending the claims that are directed to the same invention so they are no longer coextensive in scope. The filing of a terminal disclaimer cannot overcome a double patenting rejection based upon 35 U.S.C. 101.
Claims 1, 26, 31, 40-43, 52-56 are provisionally rejected under 35 U.S.C. 101 as claiming the same invention as that of claim 1, 14, 28, 29, 30, 31, 34, 47, 49, 51, 53, 54, 59, and 60 of copending Application No. 17/396,378.
Regarding the instant and copending applications, claim 1 and listed dependent claims of both applications recite a method of treating an individual or subject with an infection of HBV with a pharmaceutical composition that is of identical structure. Though the instant application recites chronic HBV and a patient with renal impairment compared to a human subject infected with HBV as stated in the copending application , it is evidenced by Deray (as described above), that individuals who are infected with the HBV virus develop chronic HBV and mild renal impairment. Furthermore, the specification of the instant application provides the broadest interpretation of a subject to include a human subject (see paragraph 0036 of the instant specification).
This is a provisional statutory double patenting rejection since the claims directed to the same invention have not in fact been patented.
Conclusion
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to DAVID YU whose telephone number is (571)272-1118. The examiner can normally be reached Monday-Friday 7:30 am -5 pm.
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/D.T.Y./Examiner, Art Unit 1635
/RAM R SHUKLA/Supervisory Patent Examiner, Art Unit 1635
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