DETAILED ACTION
1. The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
2 Applicant's amendment, filed on 06/20/2024, is acknowledged.
3. Claims 1-15, 18-28, 31-42 and 44 are pending.
4. Applicant’s election without traverse of Group I, claims 1-15, 18-28, and 31-42 directed to a method of treating or inhibiting the growth of a tumor comprising selecting an immunosuppressed or immunocompromised cancer patient and administering a PD-1 inhibitor and the species of (i) history of solid organ transplant; and (ii) cutaneous squamous cell carcinoma (CSCC), filed on 06/20/2024, is acknowledged.
5. Claims 7-8, 10-14, 44 is withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to nonelected inventions.
6. Claims 1-6, 9, 15, 18-28, and 31-42 are under examination as they read on a method of treating or inhibiting the growth of a tumor comprising selecting an immunosuppressed or immunocompromised cancer patient and administering a PD-1 inhibitor and the species of (i) history of solid organ transplant; and (ii) cutaneous squamous cell carcinoma (CSCC).
7. Applicant’s IDS, filed 09/21/2023 and 06/24/2026, is acknowledged.
8. 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.
9. Claims 1-6, 18-28, and 31-34, 36-39, 42 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by NCT03836105 (Viewing V7 (2020-07-08)).
The `105 Trial describes: (A) the effectiveness of cemiplimab (comprising the claimed SEQ ID NO) in immunosuppressed and immunocompetent patients with advanced CSCC, regardless of etiology, per available data. (B) the effectiveness of cemiplimab after prior exposure to radiation therapy for CSCC per available data. (C) the effectiveness of cemiplimab as a first-line (1L) or later systemic treatment in patients with advanced CSCC, regardless of etiology, per available data and (D) the effectiveness of cemiplimab 350 mg administered every 3 weeks (Q3W) for treatment of patients with advanced CSCC in real-world clinical settings (see Brief Summary).
The functions recited in the wherein clause flow naturally from the teachings of the prior art. Ex parte Obiaya, 227 USPQ 58, 60 (Bd. Pat. App. & Inter. 1985 (“The fact that appellant has recognized another advantage which would flow naturally from following the suggestion of the prior art cannot be the basis for patentability when the differences would otherwise be obvious.”), and Atlas Powder Co. v. Ireco Inc., 190 F.3d 1342, 1347 (Fed. Cir. 1999) (“[T]he discovery of... a scientific explanation for the prior art's functioning, does not render the old composition patentably new to the discoverer.”)). Here, the recited functional outcome recited in claims 31-33, would naturally and necessarily flow from the administration of cemiplimab. Accordingly, the prior art teaches the same method, the product used in the reference method are the same as the claimed method. Therefore, the claimed functional outcome would naturally and necessarily flow the administration of cemiplimab in treating CSCC in a human subject.
The reference teachings anticipate the claimed invention.
10. Claims 1-6, 9, 18-28, and 31-34, 36-39, 42 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Rabinowits et al. J Clin Oncol 39, 9547(May 2021) abs 9547).
Rabinowits et al teach immunosuppressed and/or immunocompromised patients are at increased risk for solid tumors and cutaneous malignancies. Limited data exist on the safety and effectiveness of immune checkpoint inhibitors (ICIs) in these patients because they are frequently excluded from clinical trials. Rabinowits et al describe the safety and effectiveness results from the initial cohort of immunosuppressed and/or immunocompromised patients with advanced cutaneous squamous cell carcinoma (CSCC) enrolled in the C.A.S.E. study (NCT03836105). C.A.S.E. is a prospective, real-world, multi-center, longitudinal study evaluating the effectiveness, safety, quality of life, and survivorship in patients with advanced CSCC treated with cemiplimab (comprising the claimed SEQ ID NO). Patients received cemiplimab 350 mg intravenously every 3 weeks per routine standard of care. Patient demographics, disease characteristics, immunosuppression, and relevant medical history were collected. Immunosuppressive regimens varied amongst patients. Investigator assessment of objective response rate (ORR), safety, and tolerability was conducted. Data from 26 immunosuppressed and/or immunocompromised patients with advanced CSCC treated with cemiplimab are presented. Recruitment is ongoing. Rabinowits et al teach that 121 patients were enrolled in the C.A.S.E. study, of which 26 patients (median age: 74 years [IQR: 71-84]; 85% male; 89% Caucasian) were designated as immunocompromised or immunosuppressed due to a history of solid organ transplant (n = 6), autoimmune disorder (n = 11), or hematologic malignancy (n = 9). Median duration of cemiplimab exposure was 14 months (IQR: 9.1–42, range: 0, 67). Among 19 immunocompromised or immunosuppressed patients who enrolled in C.A.S.E. prior to their third dose of cemiplimab, ORR per investigator assessment was 47% (95% CI: 24–71); 1 (5%) patient had complete response; 8 (42%) had partial response. One patient had a treatment-related serious adverse reaction of organ transplant rejection. One (3.8%) patient discontinued treatment due to increased alanine aminotransferase (not treatment-related). Immune-related AEs (irAEs) occurred in 23% of patients. No treatment-related AEs led to death. Rabinowits et al concluded that the safety, tolerability, and effectiveness of cemiplimab in this initial cohort of immunosuppressed and/or immunocompromised patients with advanced CSCC appear to be consistent with those observed in clinical trials that excluded these patients. Further follow-up and additional data would add to our general understanding of safety and effectiveness of anti-PD1 therapy in immunocompromised and/or immunosuppressed patient populations overall. Clinical trial information: NCT03836105. (see the entire document).
The functions recited in the wherein clause flow naturally from the teachings of the prior art. Ex parte Obiaya, 227 USPQ 58, 60 (Bd. Pat. App. & Inter. 1985 (“The fact that appellant has recognized another advantage which would flow naturally from following the suggestion of the prior art cannot be the basis for patentability when the differences would otherwise be obvious.”), and Atlas Powder Co. v. Ireco Inc., 190 F.3d 1342, 1347 (Fed. Cir. 1999) (“[T]he discovery of... a scientific explanation for the prior art's functioning, does not render the old composition patentably new to the discoverer.”)). Here, the recited functional outcome recited in claims 31-33, would naturally and necessarily flow from the administration of cemiplimab. Accordingly, the prior art teaches the same method, the product used in the reference method are the same as the claimed method. Therefore, the claimed functional outcome would naturally and necessarily flow the administration of cemiplimab in treating CSCC in a human subject.
The reference teachings anticipate the claimed invention.
11. Claims 1-6, 9, 15 18-28, and 31-39 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Paoluzzi L et al, (Current oncology (Toronto, Ont.), (19 Jan 2021) Vol. 28, No.1, pp. 574-580).
Paoluzzi teaches that immunotherapies directed at T-cell activation through antibodies targeting checkpoint proteins, such as programmed cell death 1 (PD1), are rapidly becoming the new standard of care in the treatment of several malignancies. Cemiplimab (comprising the claimed SEQ ID NOs) is a monoclonal antibody targeting PD1 that has recently emerged as a highly active treatment for locally advanced and metastatic cutaneous squamous cell carcinoma (CSCC). Patients who have received an organ transplant (OTRs) have been traditionally excluded from clinical trials with checkpoint inhibitors (CIs), given concerns for organ rejection. Renal transplant recipients (RTRs) are more likely to develop cancers than the general population, and skin cancers are among the most frequent malignancies. Paoluzzi reports the case of a 72-year-old man with a history of a kidney transplant who presented with a rapidly growing, locally advanced squamous cell carcinoma (SCC) of the scalp that recurred within four weeks from surgical resection. The patient was able to safely receive ten cycles of cemiplimab so far with significant clinical benefit, and no issues with his kidney function, while continuing immunosuppression with low dose prednisone alone. An ongoing clinical trial (NCT04339062) is further exploring the safety of CIs in patients with metastatic CSCC who have previously received allogeneic hematopoietic stem cell transplant or a kidney transplant (abstract). The patient had extensive local SCC involving the majority of his scalp, with no evidence on examination or imaging for either regional or metastatic disease. MRI of the brain and neck was done and showed irregularly enhancing scalp lesions without evidence of adjacent osseous or intracranial extension (largest lesion was 4.7 cm by 3.4 cm (Figure 1A)). After further multidisciplinary discussion with the surgical and transplant teams, given the fact he was not a candidate for any aggressive regimen due to his performance status, decision was made for immunotherapy with cemiplimab 350 mg IV every 3 weeks (see section 2). Overall, the patient has tolerated this drug very well so far without any significant issues. Paoluzzi et al teacht that recently reported successful administration of cemiplimab to an 81-year-old patient with advanced CSCC on sirolimus and prednisone for immunosuppression after renal transplantation. Sirolimus is a known inhibitor of the mechanistic target of rapamycin (mTOR). Interestingly, mTOR inhibitors have been shown to reduce the growth and proliferation of tumor cells in vitro and in vivo mouse models (section 3).
The functions recited in the wherein clause flow naturally from the teachings of the prior art. Ex parte Obiaya, 227 USPQ 58, 60 (Bd. Pat. App. & Inter. 1985 (“The fact that appellant has recognized another advantage which would flow naturally from following the suggestion of the prior art cannot be the basis for patentability when the differences would otherwise be obvious.”), and Atlas Powder Co. v. Ireco Inc., 190 F.3d 1342, 1347 (Fed. Cir. 1999) (“[T]he discovery of... a scientific explanation for the prior art's functioning, does not render the old composition patentably new to the discoverer.”)). Here, the recited functional outcome recited in claims 31-33, would naturally and necessarily flow from the administration of cemiplimab. Accordingly, the prior art teaches the same method, the product used in the reference method are the same as the claimed method. Therefore, the claimed functional outcome would naturally and necessarily flow the administration of cemiplimab in treating CSCC in a human subject.
The reference teachings anticipate the claimed invention.
12. Claims 1-6, 9, 15 18-28, 31-39 and 42 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by NCT04339062 (Cemiplimab in AlloSCT/SOT Recipients With CSCC (CONTRAC), 2020-04-08).
The `062 trial teaches that Cemiplimab is being evaluated as a treatment for advanced cutaneous squamous cell carcinoma in participants who have previously received an allogeneic hematopoietic stem cell transplant or kidney transplant involving cemiplimab, everolimus or sirolimus and prednisone (see Brief Summary). Cemiplimab is a human monoclonal anti-PD-1 antibody that works by blocking the programmed death-1 (PD-1), a cell receptor on immune cells that is involved in preventing immune cells from destroying other cells. Blocking the receptor is expected to help immune cells attack cancer cells (Detailed Description). Participants will be divided into two groups (cohorts) of allogeneic hematopoietic stem cell recipients or kidney transplants recipients. Allogeneic hematopoietic stem cell recipients will only receive the study treatment drug of Cemiplimab. Kidney transplant recipients will receive the study treatment drug of Cemiplimab along with the immunosuppressant drugs of Everolimus or Sirolimus and Prednisone to prevent kidney rejection. Participants who received allogeneic hematopoietic stem cell transplant. The administration of cemiplimab via IV, flat predetermined dosage every 21 days.
Cohort 2 Cemiplimab + Everolimus/Sirolimus + Prednisone. Participants who received a kidney transplant will receive. Cemiplimab via IV (intravenously), flat predetermined dosage every 21 days
Everolimus or Sirolimus-least 7-10 days prior to receiving the first dose of cemiplimab (Cycle 1, Day 1) and then daily while receiving Cemiplimab. Prednisone 40 mg orally the day prior to the start of cemiplimab dosing (Cycle 1, Day 1) and then daily at tapering doses while receiving Cemiplimab (Arms and Interventions).
The reference teachings anticipate the claimed invention.
13. 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.
14. Claims 40-41 are rejected under 35 U.S.C. 103 as being unpatentable over NCT03836105, NCT04339062, Rabinowits et al. J Clin Oncol 39, 9547(May 2021) abs 9547), Paoluzzi L et al, (Current oncology (Toronto, Ont.), (19 Jan 2021), 28(1):574-580), as applied to claims 1-6, 9, 15 18-28, 31-39 and 42, above and further in view of Rischin et al (Journal for ImmunoTherapy of Cancer 2020;8:e000775).
The teachings of NCT03836105, NCT04339062, Rabinowits et al and Paoluzzi et al have been discussed, supra.
The reference teachings differ from the claimed invention only in the recitation of a dose of 1 mg/kg to 20 mg/kg or, 1 mg/kg, 3 mg/kg, 10 mg/kg in claims 40-41.
Rischin et al report the primary analysis of fixed dose cemiplimab 350 mg intravenously every 3 weeks (Q3W) (Group 3) and provide a longer- term update after the primary analysis of weight- based cemiplimab 3 mg/kg intravenously every 2 weeks (Q2W) (Group 1) among metastatic CSCC (mCSCC) patients in the pivotal study (NCT02760498). Rischin et al teaches in patients with mCSCC, cemiplimab 350 mg intravenously Q3W produced substantial antitumor activity with durable response and an acceptable safety profile. Follow- up data of cemiplimab 3 mg/kg intravenously Q2W demonstrate ongoing durability of responses (abstract). Rischin et al concluded that cemiplimab 350 mg intravenously Q3W produced substantial antitumor activity. Durable responses have been observed in both weight- based and fixed- dosing groups. The safety profile was similar in both groups. Long- term follow- up of these patients is ongoing.
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to use the weight-based dose of 3 mg/kg of cemiplimab taught by Rischin int the treatments taught by NCT03836105, NCT04339062, Rabinowits et al and Paoluzzi et al because both weight-based and fixed-dose regimens were effective.
From the combined teachings of the references, it is apparent that one of ordinary skill in the art would have had a reasonable expectation of success in producing the claimed invention. Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in the art at the time the invention was made, as evidenced by the references, especially in the absence of evidence to the contrary.
14. Claims 1-6, 9, 15, 18-28, and 31-42 are rejected under 35 U.S.C. 103 as being unpatentable over Lipson et al (N Engl J Med 374;9 nejm.org March 3, 2016, IDS) in view of US Pat. 10457725 (of record).
Lipson et al teaches tumor regression and allograft rejection after administration of anti–PD-1. Lipson et al report a case in which PD-1 antibody was administered to a solid-organ transplant recipient with metastatic cutaneous squamous-cell carcinoma. The patient had a robust antitumor response along with allograft rejection. This case suggests that anti–PD-1 can be highly effective against cancers arising in the context of chronic immunosuppression including cyclosporine and prednisone. It also suggests that the PD-1 path way may be critical in maintaining the partial tolerance that prevents T-cell–mediated allograft rejection. Liposon et al teach that the patient’s cutaneous squamous-cell carcinoma progressed, first during cetuximab therapy and then during trametinib therapy (her tumor contained a loss-of function mutation in NF1). Lipson et al teach that the risk of immune-related toxic effects associated with anti–PD-1, including kidney allograft rejection, were explicitly conveyed to the patient. With the endorsement of a virtual tumor board convened to evaluate relative risk and benefit, she began pembrolizumab (anti PD-1) in September 2014. Two months after initiation of anti–PD-1, the patient had acute allograft rejection. Despite administration of high-dose glucocorticoids, the patient’s transplanted kidney did not recover. Histologic and immunohistochemical evaluation of the explanted kidney revealed severe acute and chronic cell-mediated rejection (Fig. 1). Computed tomography performed 8 months after the initiation of pembrolizumab revealed an 85% reduction in tumor burden. The patient has not had autoimmune toxic effects. She is undergoing hemodialysis without unacceptable adverse events, and her ECOG performance status has returned to 0.
The reference teachings differ from the instant claim only in the recitation that the anti-PD-1 antibody is Cemiplimab (REGN2810) (i.e., comprising the CDRs of SEQ ID NOs: 3-8), the doses and frequences and route of administrations recited in claims 36-42.
The `725 patent methods of treating or inhibiting the growth of a tumor comprising: (a) selecting a patient with cutaneous squamous cell carcinoma (CSCC); and (b) administering to the patient a therapeutically effective amount of an antibody or antigen-binding fragment thereof that specifically binds PD-1, wherein the therapeutically effective amount is administered once every two weeks in a dose comprising 1 to 3 mg/kg of the patient's body weight; wherein the anti-PD-1 antibody or antigen-binding fragment thereof comprises three heavy chain complementarity determining regions (HCDR1, HCDR2 and HCDR3) of a heavy chain variable region (HCVR) comprising the amino acid sequence of SEQ ID NO: 1 (comprising the claimed CDR sequences) and three light chain complementarity determining regions (LCDR1, LCDR2 and LCDR3) of a light chain variable region (LCVR) comprising the amino acid sequence of SEQ ID NO: 2 (comprising the claimed CDR sequences), wherein the CSCC is metastatic, unresectable and/or locally advanced, wherein the patient is intolerant to or the CSCC progresses after prior treatment with an anti-cancer therapy, wherein the CSCC is metastatic CSCC, and wherein said patient has been treated with at least one prior anti-cancer therapy selected from the group consisting of surgery, radiation, chemotherapy, and another anti-PD-1 antibody, wherein the patient is resistant or inadequately responsive to, or relapsed after prior therapy, wherein HCDR1 comprises the amino acid sequence of SEQ ID NO: 3; HCDR2 comprises the amino acid sequence of SEQ ID NO: 4; HCDR3 comprises the amino acid sequence of SEQ ID NO: 5; LCDR1 comprises the amino acid sequence of SEQ ID NO: 6; LCDR2 comprises the amino acid sequence of SEQ ID NO: 7; and LCDR3 comprises the amino acid sequence of SEQ ID NO: 8, further comprising administering to the patient an additional therapeutic agent or therapy, wherein the additional therapeutic agent or therapy is selected from the group consisting of surgery, radiation, a chemotherapeutic agent, a cancer vaccine, a programmed death ligand 1 (PD-L1) inhibitor, a lymphocyte activation gene 3 (LAG3) inhibitor, a cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) inhibitor, a T-cell immunoglobulin and mucin-domain containing-3 (TIM3) inhibitor, a B- and T-lymphocyte attenuator (BTLA) inhibitor, a T cell immunoreceptor with Ig and ITIM domains (TIGIT) inhibitor, a CD47 inhibitor, an indoleamine-2,3-dioxygenase (IDO) inhibitor, a bispecific anti-CD3/anti-CD20 antibody, a vascular endothelial growth factor (VEGF) antagonist, an angiopoietin-2 (Ang2) inhibitor, a transforming growth factor beta (TGFβ) inhibitor, a CD38 inhibitor, an epidermal growth factor receptor (EGFR) inhibitor, granulocyte-macrophage colony-stimulating factor (GM-CSF), cyclophosphamide, an antibody to a tumor-specific antigen, Bacillus Calmette-Guerin vaccine, a cytotoxin, an interleukin 6 receptor (IL-6R) inhibitor, an interleukin 4 receptor (IL-4R) inhibitor, an IL-10 inhibitor, IL-2, IL-7, IL-21, IL-15, an antibody-drug conjugate, an anti-inflammatory drug, and a dietary supplement, wherein the anti-PD-1 antibody comprises a heavy chain comprising the amino acid sequence of SEQ ID NO: 9 and a light chain comprising the amino acid sequence of SEQ ID NO: 10 (see claims 1-18) (i.e., REGN2810) (see col., 23, lines 45+).
Those of skill in the art would have had reason to use the REGN2810 of the '725 patent as a substitute for the anti-PD-1 antibody treatment taught in WO 98/14192 because, like the anti-PD-1 antibody taught in Lipson et al, REGN2810 binds to PD-1 and treat cutaneous squamous cell carcinoma (CSCC). Substituting a known element for another, to yield the known result, is obvious. See KSR, 550 U.S. at 416, 421 (2007).
"[W]hen a patent claims a structure already known in the prior art that is altered by the mere substitution of one element for another known in the field, the combination must do more than yield a predictable result." KSR Int'l v. Teleflex Inc., 550 U.S. 398,416 (2007).
"Structural similarity, alone, may be sufficient to give rise to an expectation that compounds similar in structure will have similar properties." In re Merck & Co., Inc., 231 USPQ 375,379.
Claims 36-42 are included because it would be conventional and within the skill of the art to : (i) determine an effective amount of Cemiplimab; and (ii) determine the optimum duration and means of administration. Further, it has been held that where the general conditions of a claim are disclosed in the prior art, discovering the optimum or workable ranges involves only routine skill in the art. In re Aller, 220 F2d 454,456,105 USPQ 233; 235 (CCPA 1955). see MPEP § 2144.05 part II A. The determination of the exact doses in view of the patient’s conditions and the desired frequency is well within the skilled artisan. see also In re Peterson, 315 F.3d 1325 (Fed. Cir. 2003). “Only if the “results of optimizing a variable” are “unexpectedly good” can a patent be obtained for the claimed critical range.” In re Geisler, 116 F.3d 1465, 1469 (Fed. Cir. 1997) (quoting In re Antonie, 559 F.2d 618, 620 (CCPA 1997)). “Discovery of an optimum value of a result effective variable in a known process is ordinarily within the skill of the art.” In re Boesch, 617 F.2d 272, 276 (CCPA 1980).
The claimed functional outcome the administration in claims 31-33 would be expected by the treatment with Cemiplimab in absence of evidence to the contrary.
From the combined teachings of the references, it is apparent that one of ordinary skill in the art would have had a reasonable expectation of success in producing the claimed invention. Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in the art at the time the invention was made, as evidenced by the references, especially in the absence of evidence to the contrary.
16. No claim is allowed.
17. The art made of record and not relied upon is considered pertinent to applicant's disclosure:
(i) Cowey et al. (J Clin Oncol 37, e21033(2019)).
Cowey et al teaches Advanced CSCC is a term that encompasses the locally advanced (laCSCC) and metastatic (mCSCC) condition. For advanced CSCC patients who receive conventional anticancer systemic treatment, there are limited data regarding treatment patterns and clinical outcomes. Methods: This was a retrospective, observational study of adult patients with laCSCC and mCSCC who initiated first-line (1L) systemic treatment from 1/1/2008 to 12/31/2015, with follow-up to 9/30/2017. Data were abstracted from the US Oncology Network’s iKnowMedSM electronic health record database, supplemented by chart review. ECOG performance status (PS) of 0 or 1 was required for inclusion. Exclusion criteria included tumor of unknown primary site, treatment with an anti-PD-1/anti-PD-L1 agent, participation in clinical trial, and concurrent primary cancer. Duration of therapy (DOT) and overall survival (OS) were analyzed by Kaplan-Meier method. Response rate was calculated as the proportion of patients who achieved physician assessed-response. Results: 82 patients met inclusion criteria (17 laCSCC and 65 mCSCC). Median age at start of 1L treatment was 75y; 85% were male, 79% Caucasian, 88% of patients had an ECOG PS of 1, 90% had prior surgery, 84% prior radiotherapy, and 8.5% had prior organ transplant. The most common 1L regimens were carboplatin + paclitaxel (27% of patients) and cetuximab monotherapy (24%). Median 1L DOT was 2.4 mo for the overall population; 4.1 mo for laCSCC, 2.3 mo for mCSCC. Physician-assessed response rate for 1L therapy was 18.3% overall; 17.6% for laCSCC, and 18.5% for mCSCC. Median OS from the start of 1L treatment was 15.3 mo (95% CI, 10.4-21.0) overall; 16.2 mo for laCSCC, and 15.3 mo for mCSCC. Only 24 patients (29%) received 2L therapy. Conclusions: This is the largest retrospective data set regarding advanced CSCC patients treated with conventional chemotherapy. Efficacy was low in both laCSCC and mCSCC. These data provide historic benchmarks for outcomes in advanced CSCC patients prior to the FDA approval of cemiplimab-rwlc.
18. Any inquiry concerning this communication or earlier communications from the examiner should be directed to MAHER M HADDAD whose telephone number is (571)272-0845. The examiner can normally be reached on Monday-Friday from7:00AM to 4:30PM. If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Misook Yu, can be reached at telephone number 571-272-0839. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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July 3, 2026
/MAHER M HADDAD/ Primary Examiner, Art Unit 1641
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