Ex Parte Frenette et al

Patent Trial and Appeal BoardMar 11, 2019

10980496 (P.T.A.B. Mar. 11, 2019)

UNITED STA TES p A TENT AND TRADEMARK OFFICE APPLICATION NO. FILING DATE 10/980,496 11/03/2004 125761 7590 03/13/2019 Marshall, Gerstein & Borun LLP (Icahn) 233 South Wacker Drive 6300 Willis Tower Chicago, IL 60606-6357 FIRST NAMED INVENTOR Paul S. Frenette UNITED STATES DEPARTMENT OF COMMERCE United States Patent and Trademark Office Address: COMMISSIONER FOR PATENTS P.O. Box 1450 Alexandria, Virginia 22313-1450 www .uspto.gov ATTORNEY DOCKET NO. CONFIRMATION NO. 29636/44650 5968 EXAMINER POPA, ILEANA ART UNIT PAPER NUMBER 1633 NOTIFICATION DATE DELIVERY MODE 03/13/2019 ELECTRONIC Please find below and/or attached an Office communication concerning this application or proceeding. The time period for reply, if any, is set in the attached communication. Notice of the Office communication was sent electronically on above-indicated "Notification Date" to the following e-mail address(es): mgbdocket@marshallip.com PTOL-90A (Rev. 04/07) UNITED STATES PATENT AND TRADEMARK OFFICE BEFORE THE PATENT TRIAL AND APPEAL BOARD Ex parte PAUL S. FRENETTE, BARRY S. COLLER, and ASLIHAN TURHAN Appeal 2017-004911 1 Application 10/980,4962 Technology Center 1600 Before DONALD E. ADAMS, ERIC B. GRIMES, and RYAN H. FLAX, Administrative Patent Judges. ADAMS, Administrative Patent Judge. DECISION ON APPEAL This Appeal under 35 U.S.C. Â§ 134(a) involves claim 36 (see Final Act. 3 2). Examiner entered a rejection under 35 U.S.C. Â§ 103(a). We have jurisdiction under 35 U.S.C. Â§ 6(b ). We REVERSE. 1 Oral Hearing held January 3, 2018. 2 Appellants identify "Icahn School of Medicine at Mount Sinai, formerly Mount Sinai School of Medicine ofNew York University" as the real party in interest (App. Br. 3). 3 Examiner's February 6, 2015 Final Office Action. Appeal 2017-004911 Application 10/980,496 STATEMENT OF THE CASE Appellants' disclosure "relates to methods for treating sickle cell disease in which adherence between sickled erythrocytes and leukocytes is inhibited" (Spec. ,r 1). Appellants' claim 36 is reproduced below: 36. A method of treating a sickle cell disease subject in vaso- occlusive crisis comprising administering an E-selectin inhibitor that interacts with a calcium-binding lectin domain of E-selectin in an amount effective to treat the subject. (App. Br. 4 A-1.) Ground of rejection before this Panel for review: Claim 36 stands rejected under 35 U.S.C. Â§ 103(a) as unpatentable over the combination of Pinsky, 5 Lonergan, 6 Kansas, 7 and Erbe. 8 ISSUE Does the preponderance of evidence relied upon by Examiner support a conclusion of obviousness? FACTUAL FINDINGS (FF) FF 1. Lonergan discloses that "[ s ]ickle cell anemia (SCA) is a hemolytic anemia characterized by abnormally shaped (sickled) red blood cells (RBCs ), which are removed from the circulation and destroyed at increased rates, leading to anemia" (Lonergan 972, col. 1, 11. 1-5; see Final Act. 4). 4 Appellants' May 12, 2016 Appeal Brief. 5 Pinsky et al., WO 98/13058, published Apr. 2, 1998. 6 Lonergan et al., Sickle Cell Anemia, 21 AFIP ARCHIVES 971-94 (2001). 7 Kansas, Selectins and Their Ligands: Current Concepts and Controversies, 88 BLOOD 3259-87 (1996). 8 Erbe et al., Identification of an E-selectin Region Critical for Carbohydrate Recognition and Cell Adhesion, 119 J. CELL BIOL. 215-27 (1992). 2 Appeal 2017-004911 Application 10/980,496 FF 2. Lonergan discloses that "sickled RBCs cause vascular occlusion, which leads to tissue ischemia and infarction" (Lonergan 972, col. 1, 11. 5-7; see Final Act. 4; see also Spec. ,r 2 ("vascular occlusion, producing tissue ischemia and infarction represents a major cause of morbidity and mortality among sickle cell disease patients"); 2010 Frenette Dec. 9 ,r 5 ("A vaso- occlusive crisis associated with sickle cell disease arises when leukocytes adhere to endothelial cells via E- and/or P-selectin")). FF 3. Lonergan discloses that "deformed RBCs tend to adhere to endothelium, worsening vascular occlusion, ischemia, and the likelihood of tissue infarction" (Lonergan 972, col. 1, 11. 16-18; see Final Act. 4). FF 4. Lonergan discloses that "[ f]or the vast majority of patients with SCA, the vaso-occlusive complications of the disease are much more clinically troublesome than is the anemia, which is usually well tolerated" (Lonergan 972, col. 1, 11. 18-21 ( endnote omitted); see Final Act. 4 ). FF 5. Lonergan discloses that "[a]cute, painful vaso-occlusive crises are the most common, and earliest, clinical manifestations of SCA," wherein "[t]he pain is usually described as bone pain," and are "presumed to be caused by microvascular occlusion with subsequent tissue ischemia" (Lonergan 974, col. 2, 11. 3-10; see Final Act. 4). FF 6. Lonergan discloses that "vaso-occlusive crises most commonly manifest as dactylitis, a painful swelling of the hands, fingers, feet, and toes" (Lonergan 97 4, col. 2, 11. 11-13 ( endnote omitted); see Final Act. 4 ). 9 Declaration of Paul S. Frenette, M.D., signed July 22, 2010. 3 Appeal 2017-004911 Application 10/980,496 FF 7. Pinsky: [P]rovides for a method for treating an ischemic disorder in a subject which comprises administering to the subject a pharmaceutically acceptable form of a selectin antagonist in a sufficient amount over a sufficient time period to prevent white blood cell accumulation so as to treat the ischemic disorder in the subject. (Pinsky 2:2-7 (emphasis added); see also id. at 19:3-8; Final Act. 4.) FF 8. Pinsky's "ischemic disorder may include, but is not limited to a peripheral vascular disorder, a venous thrombosis, a pulmonary embolus, a myocardial infarction, a transient ischemic attack, unstable angina, a reversible ischemic neurological deficit, sickle cell anemia or a stroke disorder" (Pinsky 19:30-34 ( emphasis added); see also id. at 21:4--1 O; Final Act. 4). FF 9. Pinsky's "selectin antagonist may be ... an antibody" (Pinsky 19:8- 11; see Final Act. 4). FF 10. Pinsky discloses that "[t]he selectin may be a P-selectin, an E- selectin, or an L-selectin" (Pinsky 19:11-12; see Final Act. 4). FF 11. Examiner finds that Pinsky does disclose an antibody that interacts with a calcium-binding lectin (C-lectin) domain of E-selectin and relies on Kansas and Erbe to make up for this deficiency in Pinsky (see Final Act. 4). ANALYSIS Based on the combination of Pinsky, Lonergan, Kansas, and Erbe, Examiner concludes that, at the time Appellants' invention was made, it would have been prima facie obvious "to use antibodies capable of binding to the C-lectin domain as the E-selectin antagonists in the method of Pinsky ... to achieve the predictable result of treating a SCD [ sickle cell disease] patient in vaso-occlusion crisis" (Final Act. 4; see id. (Examiner finds that 4 Appeal 2017-004911 Application 10/980,496 because "ischemia in SCD is caused by vaso-occlusion ... Pinsky ... necessarily treat[s] a SCD patient in vaso-occlusion crisis"); see FF 1-12). We are not persuaded. "[V]aso-occlusive crises are the most common, and earliest, clinical manifestations of SCA" and are "presumed to be caused by microvascular occlusion with subsequent tissue ischemia" (FF 5; see also FF 2 ("[S]ickled RBCs [ associated with SCA] cause vascular occlusion, which leads to tissue ischemia."). Thus, it is clear on this record that a vaso-occlusive crisis is associated with tissue ischemia (see FF 1-5). As Frenette makes clear, however, "[ v Jaso-occlusive crises are not continuous, or always present, in a person suffering from sickle cell disease" (2010 Frenette Dec. ,r 6). On this record, Examiner failed to establish that an ischemic disorder, which, according to Pinsky, "may include, but is not limited to ... sickle cell anemia," is limited to a vaso-occlusive crisis and/or an ischemia (see FF 8 (Pinsky's "is chemic disorder may include, but is not limited to ... sickle cell anemia; cf App. Br. 7 ("Pinsky repeatedly discloses treatment of ischemic disorders, not the treatment of an ischemia that may or may not be present in a particular patient at a given time and certainly not the treatment of vaso- occlusion as but one of the divergent causes of ischemia" ( emphasis added)); see also 2010 Frenette Dec. ,r 7 ("Pinsky does not disclose a method of treating vaso-occlusion in a subject with sickle erythrocytes by administering an inhibitor of a selectin.")). Thus, on this record, Examiner failed to establish that Pinsky's "method of treating an is chemic disorder in a subject" excludes the 5 Appeal 2017-004911 Application 10/980,496 treatment of reperfusion injury (see FF 7-10). To the contrary, as Frenette explains, notwithstanding Examiner's assertions to the contrary: Pinsky is directed to treating the post-ischemic (i.e., post- blockage) damage, or reperfusion injury, caused by recruitment of PMNs by P-selectin on the surface of endothelial cells. Any treatment described by Pinsky occurs after the blockage or ischemic event subsides and reperfusion occurs, thereby allowing PMN s to interact with the endothelial cells "downstream" of the previous blockage. In other words, Pinsky is concerned with the after-effects of an ischemic event and does not teach how to treat the blockage or prevent the blockage from occurring. In contrast, vaso-occlusion associated with sickle cell disease is caused by adherence of leukocytes to endothelial cells followed by subsequent adherence of erythrocytes to the immobilized PMNs, ultimately resulting in a vaso-occlusive crisis. The pending claims define methods of inhibiting vaso-occlusion (i.e., blockage) itself, not the after-effects of such a blockage. (2010 Frenette Dec. ,r 7 ( emphasis added).) Therefore, Frenette declares that "a person of skill in the art would not have turned to Pinsky's method of treating reperfusion injury for guidance in developing a method of treating vaso-occlusion associated with sickle cell disease" (id.; see also App. Br. 10 ("Examiner acknowledged that Pinsky does not expressly disclose treatment of a subject with SCD in vaso-occlusive crisis, and [] Examiner has not established that treating a subject with SCD inherently involves treating a subject with SCD in vaso-occlusive crisis")). We agree. Examiner failed to establish that any of Lonergan, Kansas, or Erbe, individually or in combination, make up for the foregoing deficiencies in Pinsky (see FF 1---6 and 11). 6 Appeal 2017-004911 Application 10/980,496 CONCLUSION The preponderance of evidence relied upon by Examiner fails to support a conclusion of obviousness. The rejection of claim 36 under 35 U.S.C. Â§ I03(a) as unpatentable over the combination of Pinsky, Lonergan, Kansas, and Erbe is reversed. REVERSED 7