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 .1
Status of Claims
Claims 106-125 are pending. Note that throughout the office action, the claimed compound SSR125543, a known CRF1 antagonist will be interchangeably referred by its other commonly used designation, Crinecerfont.
Election/Restrictions
Applicant’s election of the species hydrocortisone in the reply filed on 8/27/2025 is acknowledged. Because applicant did not distinctly and specifically point out the supposed errors in the restriction requirement, the election has been treated as an election without traverse (MPEP § 818.01(a)).
Claims 106-125 are under examination.
hydrocortisone (11 β, 17α,21-trihydroxypregn-4-ene-3,20-dione),
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Information Disclosure Statement
The information disclosure statements (IDS)s submitted 04/126/2024, 07/18/2024, 08/23/2024 and 11/12/2024 are in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Claim Rejections - 35 USC § 112 (Scope of Enablement)
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 106-125 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for treatment of CAH with a combination of hydrocortisone and the CRF1 antagonist, SSR125543 (aka Crinecerfont), where the steroid dosage is reduced in increments of 5 mg due to the co-administration with Crinecerfont, compared to a dosage of steroid administered alone, does not reasonably provide enablement for the full scope of the claimed method, which would entail 5 mg reductions of any steroid with concomitant CRF1 antagonist therapy.
The claimed invention is directed to a method of treating congenital adrenal hyperplasia (CAH) in a subject, comprising administering to the subject a therapeutically effective amount of Crinecerfont. SSR1255432
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CAS Reg. No. 752253-39-7
or salt thereof, at a frequency of at least twice per day, and a steroid [ANY] or a pharmaceutically acceptable salt thereof,
wherein the steroid or pharmaceutically acceptable salt thereof is administered at a reduced dosage compared to a dosage of [any] steroid or a pharmaceutically acceptable salt thereof administered alone, wherein the reduced dosage [of any steroid] is in a 5 mg increment.
The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to practice the method invention commensurate in scope with the instant claims.
Applicant’s attention is drawn to In re Wands, 8 USPQ2d 1400 (CAFC1988) at 1404 where the court set eight forth factors to consider when assessing if a disclosure would have required undue experimentation. Citing Ex parte Forman, 230 USPQ 546 (BdApls 1986) at 547 the court recited eight factors: (1) the nature of the invention; (2) the state of the prior art; (3) the relative skill of those in the art; (4) the predictability or unpredictability of the art; (5) the breadth of the claims; (6) the amount of direction or guidance presented; (7) the presence or absence of working examples; and (8) the quantity of experimentation necessary.
The predictability or unpredictability of the art:
The instant claimed invention is unpredictable since a person having ordinary skill in the art (PHOSITA) recognizes issues in CRF1 antagonism in the treatment of human subjects and the limited scope steroids that are reduced in strictly in 5 mg increments, as claimed. As a general statement, CRF1 antagonism in clinical trials is unpredictable, as per (Spierling and Zorilla) Spierling 20173, “CRF1 antagonists did not show activity in some models or conditions under which some clinically efficacious treatments do.” See page 1470, column 2.
In contrast, Newfield 20234, demonstrated successful results with claimed compound CRF1 antagonist, Crinecerfont in combination with steroid therapy for the treatment of CAH claimed, had substantial reductions in adrenal androgens and precursors, consistent with another study of Crinecerfont in adults with classic 21OHD CAH. See abstract.. However, this successful therapy with Crinecerfont only occurred with specific steroid therapy, such as hydrocortisone and prednisone, not the broad category of steroids as claimed. See Table 1, where study participants were limited to the glucocorticoids, hydrocortisone and prednisone.
Further, the unpredictability in the art is noted where not all doses of steroid activity are measured in strictly 5 mg increments, where the art provides teachings to convert doses among the different steroids to equivalent doses (se Morris 20185 Table 1 reproduced below).
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As noted above, dexamethasone and betamethasone note dose equivalents to the other steroids in increments of 0.75 mg as detailed in Table 1 of Morris 2018, and not 5 mg increments as required by the claimed method.
While a PHOSITA would easily be able to convert dose reductions among different steroids for their clinical activity, as the equivalent doses of different doses are NOT all based on 5 mg increments as specifically claimed by claim 106, the unpredictability in the art points to a lack of enablement of the full scope of the claimed invention beyond hydrocortisone and prednisone (and other steroids per measured in 5 mg increments per Morris 2018), where the claimed method steroid dose reduction is measured strictly in 5 mg increments.
Accordingly, the unpredictably in the art (at least with respect to 5 mg decreasing increments with all known steroids) is a Wands factor against enablement of the full scope of the invention.
The breadth of the claims
The instant claims are deemed broad as they are directed to co-administration of any steroid as claimed. The broad scope of the claims is a Wands factor against the enablement of the full scope of the claimed invention.
The amount of direction or guidance presented, and the presence or absence of working examples: It has been established that “the amount of guidance or direction needed to enable the invention is inversely related to the amount of knowledge in the state of the art as well as the predictability in the art.” In re Fisher, 427 F.2d 833, 839 166 USPQ 18, 24 (CCPA 1970).
There is no working example that supports the claimed invention, comprising the administration of Crinecerfont and a steroid as claimed, where ANY steroid doses are reduced in strictly 5 mg increments as claimed.
Rather, the specification merely Example 2’s clinical study, where data was generated regarding combination therapy and measurement of hormonal steroid levels with CRF1 antagonist Tildacerfont (Compound 3) and NOT claimed CRF1 antagonist Crinecerfont; and Example 3, proposing a hypothetical prophetic example with CRF1 antagonist Tildacerfont (Compound 3), NOT Crinecerfont and proposing steroid dose reduction in comparison to steroid monotherapy.
The lack of direction and working examples from the specification is a Wands factor against the enablement of the full scope of the invention.
Therefore, in view of the Wands factors as discussed above, unpredictability in the art, the breadth of the claims and lack of amount of direction or guidance presented, Applicant fails to provide information sufficient to practice the claimed invention as claimed.
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 106-111, 119-121 and 124-125 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Grigoriadis (aka US 877) (U.S. 2017/0020877)
US 877 is cited on the IDS dated Apr 16 2024, US Pat Doc 020.
The claimed invention (claim 106) is directed to a method of treating congenital adrenal hyperplasia (CAH) in a subject, comprising administering to the subject a therapeutically effective amount of SSR1255436, aka Crinecerfont or salt thereof, at a frequency of at least twice per day, and a steroid or a pharmaceutically acceptable salt thereof,
wherein the steroid or pharmaceutically acceptable salt thereof is administered at a reduced dosage compared to a dosage of steroid or a pharmaceutically acceptable salt thereof administered alone, wherein the reduced dosage [of any steroid] is in a 5 mg increment.
Regarding claim 106, US 877 teaches a method of treating CAH by administering to a subject in need thereof a CRF1 receptor antagonist having a dissociation half-life in excess of 30 minutes. See claim 1. US 877 teaches the claimed CRF1 antagonist administered is the claimed compound, SSR-125543, i.e. Crinecerfont. See claims 13 and 18. See paragraphs 13 and 54, wherein the claimed method of treating CAH patients in need comprises administering SSR-125543.
Regarding claim 106 and the limitation of administering a steroid, US 877 teaches treatment of CAH includes efforts to normalize cortisol deficiency with glucocorticoids (hydrocortisone in children) and the need to monitor treatment so as to avoid side effects of the steroids. See paragraph 47. See paragraph 50 for full detail.
Regarding claim 106 and the reduction of levels of a co-administered steroid with the CRF1 antagonist versus the steroid alone, US 877 teaches CRF1 antagonists have the potential to directly inhibit ACTH release in patients with CAH, thereby allowing normalization of androgen production while using lower, more physiologic doses of hydrocortisone, and reducing treatment-associated side effects. See paragraph 6.
Regarding the subject in need where the subject in need is receiving a combination of CRF1 antagonist and glucocorticoid (GC) steroid, requires less steroid than one receiving monotherapy of steroid, US 877 teaches “methods for treating CAH by administering a CRF1 receptor antagonist may further comprise administering a GC at a dose lower than the currently recommended dose of a GC for treating a subject who has CAH.” See paragraph 70.
AS required by claim 106 and reduction of doses of a steroid in strictly 5 mg increments, in an adult CAH patient, US 877 teaches, the dose of a GC, such as the dose of hydrocortisone (HC), prednisone, prednisolone, dexamethasone, or fludrocortisone recommended for maintenance therapy in a fully grown subject may be decreased by about 10%, 15%, 20%, 30%, 40%, 50%, 60% or more from the recommended doses of 15-25 mg/day HC [hydrocortisone] ; 5-7.5 mg/day prednisone, 4-6 mg/day prednisolone; 0.25-0.5 mg/day dexamethasone, or 0.05-0.2 mg/day of fludrocortisone.” See paragraph 30.
Regarding claim 107 and the sequential administration of hydrocortisone within about 24 hours of the steroid (glucocorticoid), US 877 teaches the dose reduction of glucocorticoid (GC) or mineralocorticoid by at least 10% to 60% from the recommended daily dose of GC, within 24 hours, such as hydrocortisone. See paragraph 30.
Regarding claims 108-109 the limitations of classic and non-classic CAH, US 877 teaches CAH patients are considered to be treated for either, classic or non-classic. See paragraph 4. While Figure 1 of US 877 teaches treatment of classical CAH in terms of 11-beta hydroxylase deficiency, a PHOSITA would readily envisage treatment of non-classical CAH, as guided by paragraph 4. Per MPEP 2131.02 III. to support the anticipation rejection, a person having ordinary skill in the art (PHOSITA) would immediately envisage treatment of both classic and non-classic versions of CAH as per the teachings of US 877, defining both CAH conditions.
Regarding claims 110-111 and the administration of a glucocorticoid steroid such as hydrocortisone, US 877 teaches CRF1 antagonists have the potential to directly inhibit ACTH release in patients with CAH, thereby allowing normalization of androgen production while using lower, more physiologic doses of hydrocortisone, and reducing treatment-associated side effects. See paragraph 6. US 877 teaches, the dose of a GC, such as the dose of hydrocortisone (HC), prednisone, prednisolone, dexamethasone, or fludrocortisone recommended for maintenance therapy in a fully grown subject may be decreased by about 10%, 15%, 20%, 30%, 40%, 50%, 60% or more from the recommended doses of 15-25 mg/day HC [hydrocortisone]. See paragraph 30.
Regarding claims 119-121 and the limitation of wherein the SSR125543 or salt thereof, is administered in a dose of about 50 mg to about 200 mg, about 200 mg or about 100 mg, total daily dose to the subject, US 877 teaches “[in] general, the amount of a compound described herein, that is present in a dose ranges from about 0.1 mg to about 30 mg per kg weight of the subject. In certain embodiments, a single dose is about 50-1000 mg. See paragraph 63.
Regarding claims 124-125 and the treatment of adult and pediatric patients, US 877 teaches treatment of CAH is based on normalization of hormone and steroid levels using a variety of medications from diagnosis in infancy through adulthood. See paragraph 44.
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.
Claims 106-121 and 123-125 are rejected under 35 U.S.C. 103 as being unpatentable over Grigoriadis (aka US 877) (US20170020877).
Regarding the invention of claim 106, US 877 teaches the claimed CRF1 antagonist administered is the claimed compound, SSR-125543, i.e. Crinecerfont to treat CAH. See claims 1, 13 and 18. See paragraphs 13 and 54, wherein the claimed method of treating CAH patients in need comprises administering SSR-125543.
Regarding claim 106 and the limitation of administering a steroid, US 877 teaches treatment of CAH includes efforts to normalize cortisol deficiency with glucocorticoids (hydrocortisone in children) and the need to monitor treatment so as to avoid side effects of the steroids. See paragraph 47. See paragraph 50 for full detail.
Regarding claim 106 and the reduction of levels of a co-administered steroid with the CRF1 antagonist versus the steroid alone, US 877 teaches CRF1 antagonists have the potential to directly inhibit ACTH release in patients with CAH, thereby allowing normalization of androgen production while using lower, more physiologic doses of hydrocortisone, and reducing treatment-associated side effects. See paragraph 6.
Regarding the subject in need where the subject in need is receiving a combination of CRF1 antagonist and glucocorticoid (GC) steroid, requires less steroid than one receiving monotherapy of steroid, US 877 teaches “methods for treating CAH by administering a CRF1 receptor antagonist may further comprise administering a GC at a dose lower than the currently recommended dose of a GC for treating a subject who has CAH.” See paragraph 70.
As required by claim 106 and reduction of doses of a steroid in strictly 5 mg increments, in an adult CAH patient, US 877 teaches, the dose of a GC, such as the dose of hydrocortisone (HC), prednisone, prednisolone, dexamethasone, or fludrocortisone recommended for maintenance therapy in a fully grown subject may be decreased by about 10%, 15%, 20%, 30%, 40%, 50%, 60% or more from the recommended doses of 15-25 mg/day HC [hydrocortisone] ; 5-7.5 mg/day prednisone, 4-6 mg/day prednisolone; 0.25-0.5 mg/day dexamethasone, or 0.05-0.2 mg/day of fludrocortisone.” See paragraph 30.
While US 877 teaches the method of claim 106 as detailed above, with regard to the particular species of claims 112-116 and those claims dependent, it does not explicitly recite the species of method where the subject has steroid hormones levels of ACTH, A4, 17-OHP, that is less than two times an upper limit of a reference range of the at least one steroid hormone level.
In terms of claim interpretation, it is pointed out that elevated reference ranges to slightly elevated above normal reference range of adrenocorticotropic hormone (ACTH), androstenedione (A4), 17-hydroxyprogesterone (17-OHP), levels would be well within the claimed limitations of less than twice the upper limit of said A4 and ACTH as per claims 112-116.
Regarding this species of claim 106, as detailed in claims 112-116, US Pub 877 teaches the need to measure ACTH, 17-OHP and A4 in a CAH subject in need. See paragraph 40-42. See also paragraphs 44-45 disclosing the need of monitoring steroid (glucocorticoid) therapy to avoid side effects, monitoring ACTH and A4. The basis to do so would be monitoring levels of these steroid hormones to adjust doses of steroid (such as hydrocortisone) in 5 mg increments as claimed. See paragraph 70.
While the art recognizes the claimed subject and claimed method administering a steroid and CRF1 antagonist, monitoring the levels of ACTH and A4 related with such therapy and noting the reduction of steroid levels in a subject taking the CRF1 antagonist, it does not specifically recite the limitations of where the monitored A4 and ACTH levels less than a two times an upper limit of a reference range of A4 or ACTH.
However, based on the teachings of US 877, the
treatment of CAH, CRF receptor antagonists would potentially block the release of ACTH from pituitary corticotrophs, thereby decreasing the production of androgens, and allow a more refined treatment paradigm for replacement of cortisol [naturally occurring equivalent of synthetic steroid hydrocortisone]. Animal and human studies have shown the pharmacologic effect of Compound I (NBI-77860) on ACTH release. Standard biomarker assessments used by endocrinologists when monitoring treatment efficacy may be used for monitoring the effects of this CRF1 receptor antagonist. Plasma levels of 17-OHP, androstenedione, testosterone, cortisol [naturally occurring hydrocortisone] and ACTH, as well as urinary metabolites of these steroids, are easily measured in both children and adults giving rapid and meaningful data regarding treatment impact.
US 877 teaches in treating CAH patients,
Optimal doses may generally be determined using experimental models and/or clinical trials. The optimal dose may depend upon the body mass, weight, or blood volume of the subject. In general, the amount of a compound described herein, that is present in a dose ranges from about 0.1 mg to about 30 mg per kg weight of the subject. In certain embodiments, a single dose is about 50-1000 mg. The use of the minimum dose that is sufficient to provide effective therapy is usually preferred. Subjects may generally be monitored for therapeutic effectiveness by clinical evaluation and using assays suitable for the condition being treated or prevented, which assays will be familiar to those having ordinary skill in the art and are described herein. The level of a compound that is administered to a subject may be monitored by determining the level of the compound in a biological fluid, for example, in the blood, blood fraction (e.g., serum), and/or in the urine, and/or other biological sample from the subject. Any method practiced in the art to detect the compound may be used to measure the level of compound during the course of a therapeutic regimen.
The dose of a composition comprising at least one of the compounds described herein for treating CAH or a related disease or disorder may depend upon the subject's condition, that is, stage of the disease, severity of symptoms caused by the disease, general health status, as well as age, gender, and weight, and other factors apparent to a person skilled in the medical art. Similarly, the dose of the compound may be determined according to parameters understood by a person skilled in the medical art. See paragraphs 63-64.
As stated above, a person having ordinary skill in the art (PHOSITA) recognizes what would be above reference standards of ACTH and A4 levels in the CAH afflicted subject in need, and would recognize the necessity of lowering concurrent steroid (hydrocortisone) treatment to avoid concomitant side effects, especially where established by US 877, co-administration of a CRF1 antagonist would achieve this goal. A PHOSITA would readily recognize that ACTH and A4 levels under twice the upper limit of a reference range inclusive of a range above normal reference range is a logical clinical target in CAH patients in need, so reduce concomitantly administered steroids, known to have adverse side effects..
Prior to the filing of the present patent application, it would have been prima facie obvious to a PHOSITA following the teachings of the teachings of US 877 with regard to co-administering a CRF1 antagonist with reduced levels of concomitant steroid (hydrocortisone) relative to a patient not taking the CRF1 antagonist, modified with other teachings of US 877 noting the ordinary skill level of a PHOSITA (physician) in order to treat patients with above normal reference ranges of ACTH and A4 (i.e. less than twice the upper limit of said range, but still above a normal reference range).
The PHOSITA would have had a reasonable expectation of success because the prior art recognizes the treatment of CAH with steroids with side effects, and an effort to reduce such side effects by co-administering a CRF1 antagonist, where a clinical goal is to reduce administered steroids to treat CAH subject with above normal reference range of ACTH and A4, such those patients with ACTH and A4 levels while less than twice the upper limit of a normal reference range, but still above a normal reference range.
Regarding claim 107 and the sequential administration of hydrocortisone within about 24 hours of the steroid (glucocorticoid), US 877 teaches the dose reduction of glucocorticoid (GC) or mineralocorticoid by at least 10% to 60% from the recommended daily dose of GC, within 24 hours, such as hydrocortisone. See paragraph 30.
Regarding claims 108-109 the limitations of classic and non-classic CAH, US 877 teaches CAH patients are considered to be treated for either, classic or non-classic. See paragraph 4. While Figure 1 of US 877 teaches treatment of classical CAH in terms of 11-beta hydroxylase deficiency, a PHOSITA would readily envisage treatment of non-classical CAH, as guided by paragraph 4. Per MPEP 2131.02 III. to support the anticipation rejection, a person having ordinary skill in the art (PHOSITA) would immediately envisage treatment of both classic and non-classic versions of CAH as per the teachings of US 877, defining both CAH conditions.
Regarding claims 110-111 and the administration of a glucocorticoid steroid such as hydrocortisone, US 877 teaches CRF1 antagonists have the potential to directly inhibit ACTH release in patients with CAH, thereby allowing normalization of androgen production while using lower, more physiologic doses of hydrocortisone, and reducing treatment-associated side effects. See paragraph 6. US 877 teaches, the dose of a GC, such as the dose of hydrocortisone (HC), prednisone, prednisolone, dexamethasone, or fludrocortisone recommended for maintenance therapy in a fully grown subject may be decreased by about 10%, 15%, 20%, 30%, 40%, 50%, 60% or more from the recommended doses of 15-25 mg/day HC [hydrocortisone]. See paragraph 30.
Regarding claims 117-118 and the levels of steroid hormone determined from biological samples (blood, blood fraction/serum, urine etc.), US 877 teaches a blood sample is used to test 17-OHP. See paragraph 41. Also see paragraph 91, where it is taught 16-hour post dose blood samples were collected in the clinical study where biomarkers such as 17-OHP, ACTH and androstenedione (A4) were noted to be of interest.
Regarding claims 119-121 and the limitation of wherein the SSR125543 or salt thereof, is administered in a dose of about 50 mg to about 200 mg, about 200 mg or about 100 mg, total daily dose to the subject, US 877 teaches “[in] general, the amount of a compound described herein, that is present in a dose ranges from about 0.1 mg to about 30 mg per kg weight of the subject. In certain embodiments, a single dose is about 50-1000 mg. See paragraph 63.
Regarding claim 123 and the testing of ACTH in the morning, US 877 teaches that ACTH release is typically at 1-2 AM. See paragraph 66. Therefore, a PHOSITA would routinely test for ACTH in the morning, either at the time of release or shortly thereafter.
Regarding claims 124-125 and the treatment of adult and pediatric patients, US 877 teaches treatment of CAH is based on normalization of hormone and steroid levels using a variety of medications from diagnosis in infancy through adulthood. See paragraph 44.
Claims 106-125 are rejected under 35 U.S.C. 103 as being unpatentable over Grigoriadis (aka US 877) (US20170020877) in view of Dhoot et al (aka US 623) (US 2006/0078623 A1). US 623 is cited on the April 16 2024 IDS as US Pat Doc 012.
As detailed above, US 877 teaches the method of claims 106-121 and 123-125 as detailed above, but does not necessarily recite the species of the claimed method (claims 1-6) with regard to claim 122 and the disclosure of the particular species CRF1 antagonist SSR125543 in the form of microparticles.
Although US 877 generally taught CRF1 receptor antagonist SSR125543 for the treatment of CAH, US 877 did not specifically teach CRF1 antagonists microparticles.
US 623 teaches a method of treating that the small size of microparticles allows for greater bioavailability of the active agent, since the size permits the particles to pass from the stomach to the small intestine, where dissolution and drug absorption is best [0004]. Active agents at a particle size of about 1 to about 999 micrometers were disclosed [0007].
Prior to the filing of the present patent application, it would have been prima facie obvious to a PHOSITA following the teachings of the primary reference US 877 to treat CAF with lesser doses of steroids due to the combination therapy with CRF1 antagonist SSR125543, modified by the teachings of US 623 to formulate US 877 SSR125543 as microparticles as taught by US 623.
The PHOSITA would have had a reasonable expectation of success because by micronizing SSR125543 at 1-999 microns, at this said diameter, the particles more
freely pass through the stomach and into the small intestine, as taught by US 623.
Conclusion and Correspondence
In summary, no claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to WILLIAM LEE whose telephone number is (571)270-3876. The examiner can normally be reached M-F.
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, Adam C. 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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/WILLIAM Y LEE/Examiner, Art Unit 1623
/ADAM C MILLIGAN/Supervisory Patent Examiner, Art Unit 1623
1 CONTINUING DATA
This application is a CON of 17/578,149 01/18/2022
17/578,149 is a CON of PCT/US2020/042820 07/20/2020
PCT/US2020/042820 has PRO 63/047,822 07/02/2020
PCT/US2020/042820 has PRO 62/876,176 07/19/2019
2 (S)-4-(2-chloro-4-methoxy-5-methylphenyl)-N-(2-cyclopropyl-1-(3-fluoro-4-methylphenyl)ethyl)-5-methyl-N-(prop-2-yn-l-yl)thiazol-2-amine
Crinecerfont
CAS#: 752253-39-7 (free base)
SSR125543;
SSR-125543;
SSR 125543;
SSR125543A;
SSR-125543A;
SSR 125543A;
3 Spierling and Zorilla Don’t stress about CRF: assessing the translational failures of CRF1antagonists Psychopharmacology (2017) 234:1467–1481
4 Newfield et al. Crinecerfont, a CRF1 Receptor Antagonist, Lowers Adrenal Androgens in Adolescents With Congenital Adrenal Hyperplasia The Journal of Clinical Endocrinology & Metabolism, Volume 108, Issue 11, November 2023, Pages 2871–2878
5 Morris Steroid-induced diabetes and hyperglycaemia. Part 1: mechanisms and risks Diabetes & Primary Care Vol 20 No 4 2018 (Year: 2018)
6 (S)-4-(2-chloro-4-methoxy-5-methylphenyl)-N-(2-cyclopropyl-1-(3-fluoro-4-methylphenyl)ethyl)-5-methyl-N-(prop-2-yn-l-yl)thiazol-2-amine
Crinecerfont
CAS#: 752253-39-7 (free base)
SSR125543;
SSR-125543;
SSR 125543;
SSR125543A;
SSR-125543A;
SSR 125543A;