PATENT
`Attorney Docket No. AGP-002
`
`IN THE UNITED STATES PATENT AND TRADEMARK OFFICE
`
`In re Patent Application of: Rader
`
`Application No.: 10/591,923
`
`Confirmation No.:5393
`
`Filed: June 21, 2007
`
`Art Unit: 1614
`
`For: Methods for Treating Disorders or Diseases
`Associated with Hyperlipidemia
`
`Examiner: K. Weddington
`
`DECLARATION OF WILLIA~M SASIELA, PH.D., UNDER 37 CFR 1.132
`
`I, William Sasiela, hereby declare as follows:
`
`1. I am Executive Vice President and Chief Medical Officer at Aegerion Pharmaceuticals, Inc,
`the licensee of the above referenced Patent Application.
`
`2. I have extensive experience in lipid metabolism and therapies for atherosclerosis and related
`diseases, as evidenced by the copy of my curriculum vitae attached as Exhibit A.
`
`3. I have read and understood the Application, including the cunently-pending claims, and the
`cited prior art patents of Biller and Gregg.
`
`4. I make this declaration in order to provide my scientific opinions and facts known to me
`which may be of assistance in the examination of the Application.
`
`5. I understand that, prior to the claimed method for treating hyperlipidemia or
`hypercholesterolemia that includes stepwise increasing dose levels, the claimed MTP
`inhibitor had been the subject ofhmnan clinical trials for the treatment of
`hypercholesterolemia, where the MTP inhibitor was administered at a constant dose level of
`25 mg/day or above. Because of adverse events that included clinically significant
`gastrointestinal steatorrhea and statistically significant hepatobiliary (elevation of liver
`function tests and fatty liver), the clinical trials and further development of the drug were
`discontinued, despite significant reduction in patient cholesterol.
`
`6. To my knowledge, few medications for treatment of hyperlipidemia or hypercholesterolemia
`are administered to patients with stepwise increasing dose levels to minimize side effects.
`For example, manufacturers of statins, the world's largest category of lipid lowering drugs,
`have not employed, to my knowledge, step wise increasing doses (titration) in order to
`minimize side effects that would otherwise be observed at high doses. Ezetimibe (Zetia®),
`another type oflipid lowering drug, was developed and received FDA approval at a single
`dose level.
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`CFAD Ex. 1010 (1 of 11)
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`7. I believe that the claimed method for treating hyperlipidemia or hypercholesterolemia that
`includes stepwise increasing dose levels as recited in claim 1 would have not been obvious to
`a person sldlled in the art at the time of the invention on the basis of any teaching of the
`Biller or Gregg patents and/or on the basis of general knowledge of those skilled in the art. I
`note that previous developers of this MTP inhibitor, who appear to have invested much
`thought and effort on the research and previous clinical trial did not rn.1.ive at a solution to the
`adverse events shown in patients at constant level dosing.
`
`8. My colleagues and I have supervised Phase I, II, and III clinical trials, including Phase II
`randomized, double-blind human clinical trials, to assess the effectiveness and rate of adverse
`events ofthe instrn.1tly claimed methods of treating hyperlipidemia or hypercholesterolemia.
`I present below a summary of findings obtained using the claimed method.
`
`9. Patients were administered low doses of the claimed MTP inhibitor (as pictorially
`represented in pending claim 1 ). Patients in study 1 were administered a constant level of 10
`mg ofthe MTP inhibitor daily for 12 weeks. Patients in study 2, which included two anns,
`2A, and 2B, were first administered 5 mg ofthe MTP inhibitor for 4 weeks, then
`administered 7.5 mg of the MTP inhibitor for 4 weeks, and then administered 10 mg of the
`MTP inhibitor for 4 more weeks. The results are depicted in Table A:
`
`Study
`(Total N)
`
`Study
`
`Study
`Duration
`
`Rate of Gl
`Discontinuations
`
`1 (260)
`
`10 mg
`
`12 weeks
`
`2A (85)
`
`5-710 mg
`
`12 weeks
`
`2B (85)
`
`3 (25)**
`
`5-710 mg+
`10 mg eze
`5760mg
`
`12 weeks
`
`78 weeks
`
`9/35
`
`2/28
`
`1/28
`
`3/25
`
`Rate of Gl
`adverse
`events
`30/35
`(85.7%)
`18/28
`(64.3%}
`12/28
`(42.9%)
`12/21
`(57.1%)
`
`Rate of
`Diarrhea
`
`23/35
`(65.7%)
`11/28
`(39.3%)
`10/28
`(35.7%)
`9/21
`(42.9%}
`
`**Adverse event rates based on analysts of21 treated patients
`Table A
`
`I 0. Patients in study 2A had a dramatic difference in the rate of patient discontinuation rate due
`to gastrointestinal (GI) effects, and in the rate of GI adverse events and dirn.Thea, as compared
`to study 1.
`
`11. Patients in study 2B, like study 2A, were also first administered 5 mg of the MTP inhibitor
`for 4 weeks, then administered 7.5 mg of the MTP inhibitor for 4 weeks, and then
`administered 10 mg of the MTP inhibitor for 4 more weeks. These patients were additionally
`administered ezetimibe (1 0 mg daily, at a constrn.1t dosage level). Surprisingly, patients
`administered both ezetimibe rn.1d the claimed MTP inhibitor, starting at a 5 mg dose level for
`four weeks, also had significantly decreased GI adverse events and diarrhea, even compared
`to patients administered constant level of 10 mg of the MTP inhibitor alone.
`
`2
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`CFAD Ex. 1010 (2 of 11)
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`12. Patients in study 3 suffer from homozygous familial hypercholesterolemia (hoFH), and were
`first administered 5 mg of the same MTP inhibitor used in study 1 and 2 for four weeks, then
`administered 1 0 mg of the MTP inhibitor for four weeks, then administered 20 mg of the
`MTP inhibitor for four weeks, then 40 mg of the MTP inhibitor for four weeks, then 60 mg
`of the MTP inhibitor, or to the highest tolerated dose.
`
`13. Surprisingly, the patients in study 3, initially administered 5 mg oj1\1TP inhibitor, and
`subsequently administered up to 60 mg of the MTP inhibitor, after escalation of dose levels
`to a mean dose level of 44 mg/day, show a lower rate of GI adverse events and diarrhea even
`as compared to the patients of study 1, who were administered a constant level of 1 0 mg of
`the MTP inhibitor.
`
`14. I believe that the reduced incidence of GI adverse events and diarrhea in the patient groups 2
`and 3, as indicated in Table A, is an unexpected result of the claimed method, especially as
`compared to administration of the same MTP inhibitor without escalating doses.
`
`15. I hereby declare that all statements made herein of my own knowledge are true and that all
`statements made on information and belief are believed to be true; and further that these
`statements were made with the knowledge that willful false statements and the like so made
`are punishable by fine or imprisonment, or both, under 18 U.S.C. 1001 and that such willful
`false statements may jeopardize the validity of the Application or any atent issued thereon.
`
`Dated: April 1, 201 0
`
`--&_L
`
`3
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`CFAD Ex. 1010 (3 of 11)
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`WILLIAM J. SASIELA, PH.D.
`124 Saxon Way
`Skillman, NJ 08558
`(609)651-3773
`bsasiela@aol.com
`
`EXECUTIVE PROFILE
`
`Strong Phase 11-Phase IV research background in the metabolic and cardiovascular therapeutic areas with
`particular interests and experience in lipids, atherosclerosis, diabetes and obesity. Research experience
`has covered many facets of development ranging phase II studies for small, orphan populations to
`multithousand, multiyear phase IIIb-IV CV event trials. Brings extensive experience in medical(cid:173)
`marketing issues surrounding both US and Worldwide pharmaceutical markets in the metabolic and CV
`therapeutic areas. Strong track record of managing and creating cross-functional teams. Experience in
`evaluating strategic opportunities with individual compounds and within overall internal development
`programs. Noted for excellent speaking and communication abilities.
`
`PROFESSIONAL EXPERIENCE
`
`2005-Present
`
`Aegerion Pharmaceuticals, Inc., Bridgewater, NJ
`Executive Vice President & Chief Medical Officer
`As the third employee to join the newly formed biotech company, had the responsibility for
`overall development strategy and programs, design of clinical trials and formation of internal
`clinical development team. Had overall responsibility for all facets of product development
`including clinical trials, manufacturing and regulatory functions.
`• Development strategy for AEGR-733 and AEGR-427 for hyperlipidemia including phase
`2 and phase 3 clinical trials as well as necessary preclinical and pharmacokinetic studies.
`• Led team that successfully designed and executed 6 phase 2/3 clinical trials and 11
`preclinical studies for AEGR-733.
`• Creation ofteams and hiring of personnel to support all developmental activities
`including clinical operations, regulatory affairs and manufacturing.
`• Development and execution of all meetings relating to the Aegerion Scientific Advisory
`Board.
`• Member of the Aegerion Executive team with participation and presentation at all
`Aegerion Board of Director meetings.
`• Significant role in all private and public financing activities.
`• Evaluation of all potential in-licensing candidates including compounds in the areas of
`type 2 diabetes (e.g. DDP-IV, long-acting insulin), dyslipidemia and cardiovascular
`disease.
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`CFAD Ex. 1010 (4 of 11)
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`Pfizer/Parke-Davis, New York, NY/Morris Plains, NJ
`
`1996-2005
`
`Senior Clinical Director/Worldwide Team Leader
`2003-2005
`Led Worldwide Medical Teams for Lipitor and the Atherosclerosis Development at Pfizer's NY
`headquarters. The latter group focused on developmental programs for in the area of lipids and
`atherosclerosis and included torcetrapib/atorvastatin program and the compounds that were
`acquired via the Esperion acquisition. During this period, worldwide revenues for Lipitor grew
`from $7.9 B (2002) to $12.2 B (2005). Also within this role, was member of cross-functional
`team that drove strategy for the entire CVME franchise within Pfizer from discovery to
`commercialization.
`• Led the overall medical program and medical/marketing strategy for Lipitor worldwide
`including the clinical trial program, sNDAs and other regulatory responses,
`country/regional medical/marketing initiatives.
`• Ensured alignment and appropriate roll-out of medical strategies between NYHQ, US and
`other key regions.
`• Played integral role in the development of the extensive phase 3 program and proposed
`labeling for torcetrapib/atorvastatin
`• Led efforts around lifecycle management for an established product (Lipitor) and an
`emerging product ( torcetrapi b/ atorvastatin)
`• Worked with Pfizer L&D team to identify and evaluate potential in-licensing candidates.
`Performed technical due diligence on compounds of interest.
`• Contributed to overall PFE strategy in CVME through activity in Therapeutic Area
`Strategy Teams. In particular, led efforts around identification and prioritization of
`enabling strategies for all CVME development areas.
`• Led a cross-functional team to develop strategies for validation of atherosclerosis
`imaging techniques and plasma biomarkers.
`• Managed multimillion dollar annual budgets for both the Lipitor and Atherosclerosis
`Development programs.
`
`Clinical Director/Lipitor Medical Team
`2000-2003
`As a member of the Lipitor Medical Team, directly oversaw key clinical trials and medical(cid:173)
`marketing strategy activities as well as contributed to the overall medical and marketing
`strategies for the brand.
`• Directly managed a number of phase Illb/IV trials such as MIRACL, REVERSAL,
`BELLES and SP ARCL including management of clinical study teams and budgets
`• Led medical-marketing initiative to handle emerging scientific issues and competitive
`threats including new market entrants, HDL-C and novel pleiotropic effects of statins.
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`CFAD Ex. 1010 (5 of 11)
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`•
`
`• Led the organization and management of the 2002 Atorvastatin Global Investigators
`Meeting (1000+ Global OL attendees)
`Initiated, developed and managed a global research awards program focused on HDL-C
`(annual budget of$1.5-2.0 MM)
`• Rolled out the results of first large scale CV event reduction data (ASCOT trial) in the
`U.S. including the sNDA application and marketing materials.
`• Oversaw development of materials for training and updating of US and Worldwide
`Lipitor field salesforce
`Independently and in conjunction with field medical colleagues, developed and
`maintained relationships with KOLs in lipids and atherosclerosis
`• Developed strategies for and gave presentations to large managed care and governmental
`organizations
`
`•
`
`Medical Liaison Specialist
`1998-2000
`In addition to maintaining regional field medical activities as described in the medical liaison
`position, chaired the Diabetes Therapeutic Strategy Group (DTSG) within the Parke-Davis
`medical liaison team. As chair of the DTSG, led or coordinated a number of activities including:
`• Coordination of medical and marketing strategies for diabetes/troglitazone between the
`Parke-Davis HQ teams and the US medical liaison team.
`• Development and management of knowledge database for the US medical liaison team in
`relation to diabetes which included an extensive, organized slide database and a medical
`literature updates.
`• An internship rotation within the Parke-Davis HQ diabetes medical team which included
`active involvement in analysis of completed clinical trials and initiation of a new clinical
`trial.
`• Training of new medical liaisons in regards to type 2 diabetes, insulin resistance and
`troglitazone.
`Involvement in national CME programs related to diabetes.
`
`•
`
`Medical Liaison/Sr. Medical Liaison
`1996-1998
`A member ofthe first group of medical liaisons at Parke-Davis. At various times covered some
`or all of the regions including Delaware, Maryland, Washington DC, Virginia and West Virginia.
`Responsible for regional medical coverage of all commercial and phase 3 products/programs at
`Parke-Davis which included hyperlipidemia (Lipitor), type 2 diabetes (Rezulin), hypertension
`(Accupril), the CNS areas of epilepsy, neuropathic pain, depression (Neurontin, Celexa and
`Dilantin).
`• Understand and develop relationships with key researchers and opinion leaders in the
`relevant therapeutic areas.
`Identification of phase II-IV research sites for HQ medical teams.
`
`•
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`CFAD Ex. 1010 (6 of 11)
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`• Facilitate independent research studies between regional opinion leaders and
`headquarters medical teams.
`• Act as a local product expert for regional physicians through one-on-one meetings and
`group presentations.
`• Provide therapeutic area and product training and support to the local sales
`representatives and managers.
`
`POST-DOCTORAL EDUCATION AND EXPERIENCE
`
`High School Science Instructor- Southern Vance High School, Henderson, NC. 1995-1996.
`Taught Physical Science, Biology and Anatomy and Physiology
`Voted Best Lecturer by the student body.
`
`Post-Doctoral Fellowship- University of North Carolina School of Medicine, Chapel Hill,
`NC. 1994-1995.
`Kathy Pryzwansky, Advisor
`Research project focused on the role of cGMP and its main intracellular receptor, cGMP(cid:173)
`dependent protein kinase (G-kinase ), in human monocytes. Specifically, worked to characterize
`the G-kinase present in human monocytes and determine the role of cGMP and G-kinase in the
`adhesion of human monocytes to serum-coated substratum.
`
`PRE-DOCTORAL EDUCATION
`
`Ph.D. - University of South Carolina School of Medicine, Columbia, South Carolina
`Experimental Pathology, 1994. Stanley Fowler, Advisor.
`Research into the biological role that macrophage-derived foam cells play in the initiation and
`progression of atherosclerotic lesions.
`
`B.S.- Virginia Polytechnic Institute and State University, Blacksburg, Virginia
`Biochemistry (Minors in Biology and Chemistry), 1987.
`
`Papers and/or chapters:
`
`PUBLICATIONS
`
`Samaha F, McKenney J, Bloedon L, Sasiela W, and Rader, D. Inhibition of Microsomal
`Triglyceride Transfer Protein Alone or in Combination with Ezetimibe in Patients with Moderate
`Hypercholesterolemia. Nature Clin Prac Cardiovasc Med. 2008 Aug;5(8):497-505.
`
`CFAD Ex. 1010 (7 of 11)
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`

`
`Libby P, Sasiela W. Plaque stabilization: Can we turn theory into evidence?
`Am J Cardiol. 2006 Dec 4;98(11A):26P-33P. Epub 2006 Oct 2.
`
`Schwartz GG, Olsson, AG, Szarek, M, Sasiela, W J. Relation of characteristics of metabolic
`syndrome to short-term prognosis and effects of intensive statin therapy after acute coronary
`syndrome: an analysis of the Myocardial Ischemia Reduction with Aggressive Cholesterol
`Lowering (MIRACL) trial.
`Diabetes Care. 2005 Oct;28(10):2508-13.
`
`Thompson JF, Man M, Johnson KJ, Wood LS, Lira ME, Lloyd DB, Banerjee P, Milos PM,
`Myrand SP, Paulauskis J, Milad MA, Sasiela WJ. An association study of 43 SNPs in 16
`candidate genes with atorvastatin response.
`Pharmacogenomics J. 2005;5(6):352-8.
`
`Olsson AG, Schwartz GG, Szarek M, Sasiela WJ, Ezekowitz MD, Ganz P, Oliver MF, Water D,
`Zeiher A. High-density lipoprotein, but not low-density lipoprotein cholesterol levels influence
`short-term prognosis after acute coronary syndrome: results from the MIRACL trial. Eur Heart
`J. 2005 Mar 11
`
`Nissen SE, Tuzcu EM, Schoenhagen P, Crowe T, Sasiela WJ, Tsai J, Orazem J, Magorien RD,
`O'Shaughnessy C, Ganz P; Reversal of Atherosclerosis with Aggressive Lipid Lowering
`(REVERSAL) Investigators. Statin therapy, LDL cholesterol, C-reactive protein, and coronary
`artery disease. N Engl J Med. 2005 Jan 6;352(1):29-38.
`
`Tsimikas S, Witztum JL, Miller ER, Sasiela WJ, Szarek M, Olsson AG, Schwartz GG;
`Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) Study
`Investigators. High-dose atorvastatin reduces total plasma levels of oxidized phospholipids and
`immune complexes present on apolipoprotein B-1 00 in patients with acute coronary syndromes
`in the MIRACL trial. Circulation. 2004 Sep 14;110(11):1406-12. Epub 2004 Sep 07.
`
`Kinlay S, Schwartz GG, Olsson AG, Rifai N, Sasiela WJ, Szarek M, Ganz P, Libby P;
`Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) Study
`Investigators. Effect of atorvastatin on risk of recurrent cardiovascular events after an acute
`coronary syndrome associated with high soluble CD40 ligand in the Myocardial Ischemia
`Reduction with Aggressive Cholesterol Lowering (MIRACL) Study. Circulation. 2004 Jul
`27;110(4):386-91. Epub 2004 Jul19.
`
`Kinlay S, Schwartz GG, Olsson AG, Rifai N, Leslie SJ, Sasiela WJ, Szarek M, Libby P, Ganz P;
`Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering Study Investigators.
`High-dose atorvastatin enhances the decline in inflammatory markers in patients with acute
`coronary syndromes in the MIRACL study. Circulation. 2003 Sep 30;108(13):1560-6. Epub
`2003 Sep 15.
`
`CFAD Ex. 1010 (8 of 11)
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`

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`Fowler, S.D., Gasque-Carter, P.D., Patillo-Adkisson,E., Sasiela, WJ and
`Xenachis, D.N. Cellular models of atherosclerosis in the young. Chapter 5:
`Hyperlipidemia in Childhood and the Development of Atherosclerosis.
`Ann. N.Y.Acad. Sci.,623:60-69, 1991.
`
`Abstracts and presentations:
`
`Bilheimer J, Crowley D, Sasiela W, Rader DJ. Menhaden Oil Ameliorates the Steatosis Caused
`by the Inhibition of Microsomal Triglyceride Transfer Protein. Presentation at the
`Arteriosclerosis, Thrombosis and Vascular Biology Meeting; April29- May 1, 2009.
`
`Samaha F, McKenney J, Bloedon L, Sasiela WJ, Rader D. Efficacy and Safety of the MTP(cid:173)
`Inhibitor, AEGR-733, as Immunotherapy and in Combination with Ezetimibe. Presentation at
`the XVI International Symposium on Drugs Affecting Lipid Metabolism; October 4-7, 2007;
`New York, NY, USA.
`
`Samaha F, McKenney J, Bloedon L, Sasiela WJ, Rader D. MTP-Inhibitor, AEGR-733, Reduces
`Body Weight in Patients with Hypercholesterolemia. Presentation at the XVI International
`Symposium on Drugs Affecting Lipid Metabolism; October 4-7, 2007; New York, NY, USA.
`
`Dunbar R, Bloedon L, Duffy D, Gadi R, Movva R, Sasiela WJ, Daniel J. Rader, Cuchel M.
`Impact of the MTP-Inhibitor, AEGR-733, On The Single-Dose Pharmacokinetics OfEzetimibe.
`Presentation at the XVI International Symposium on Drugs Affecting Lipid Metabolism;
`October 4-7, 2007; New York, NY, USA.
`
`Dunbar R, Bloedon L, Duffy D, Gadi R, Movva R, Sasiela WJ, Rader D, Cuchel M. Impact of
`the MTP-Inhibitor, AEGR-733, on the Single-Dose Pharmacokinetics ofFenofibrate.
`Presentation at the XVI International Symposium on Drugs Affecting Lipid Metabolism;
`October 4-7, 2007; New York, NY, USA.
`
`Duffy D, Bloedon L, Dunbar R, Gadi R, Movva R, Sasiela WJ, Rader D, Cuchel M. Impact of
`the MTP Inhibitor AEGR-733 on Pharmacokinetics of Statins. Presentation at the XVI
`International Symposium on Drugs Affecting Lipid Metabolism; October 4-7, 2007; New York,
`NY, USA.
`
`Samaha FF, McKenney J, Bloedon L, Sasiela WJ, Rader DJ. Efficacy and Safety of the MTP(cid:173)
`inhibitor, AEGR-733, as Monotherapy and in Combination with Ezetimibe. Circulation.
`2006;114:II_289.
`
`Schwartz GG, Olsson AG, Chaitman B, Goldberger J, Szarek M, Sasiela WJ. Effect oflntensive
`Statin Treatment on the Occurrence of Atrial Fibrillation after Acute Coronary Syndrome: An
`Analysis of the MIRACL Trial. Presentation at the 77th Scientific Sessions of the American
`Heart Association; November 7-10, 2004; New Orleans, LA, USA.
`
`Sasiela WJ, Silbershatz H, Szarek M. Analysis of the Renal Safety of Atorvastatin in a Broad
`Spectrum of Patients with Dyslipidemia. Poster presentation at the 74th Congress of the
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`CFAD Ex. 1010 (9 of 11)
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`European Atherosclerosis Society; April 17-20, 2004; Seville, Spain.
`
`Sasiela WJ, Silbershatz H, Ma J, Villagio E. Effect of Atorvastatin on Lipoprotein Subfraction
`Profiles in Patients with Dyslipidemia. Poster presentation at the 74th Congress of the European
`Atherosclerosis Society; April 17-20, 2004; Seville, Spain.
`
`Sasiela WJ, Silbershatz H, Szarek M. Analysis of the Renal Safety of Atorvastatin in a Broad
`Spectrum of Patients with Dyslipidemia. Poster presentation at the 53rd Annual Scientific
`Sessions ofthe American College of Cardiology; March 7-10, 2004; New Orleans, LA, USA.
`
`Tsimikas S, Witztum JL, Miller ER, Sasiela WJ, Szarek M, Olsson AG, Schwartz GG.
`Circulating Oxidized LDL Markers Reflect the Clinical Benefit Noted with Atorvastatin in the
`Myocardial Ischemia Reduction with Aggressive Lipid Lowering Therapy (MIRACL) Trial.
`Presentation at the 76th Scientific Sessions of the American Heart Association; 9-12 November,
`2003; Orlando, FL, USA.
`
`Kinlay S, Schwartz GG, Olsson AG, Rifai N, Sasiela WJ, Szarek M, Libby P, Ganz P. Soluble
`CD40L, Recurrent Cardiac Events, and Atorvastatin in the MIRACL Study. Poster presentation
`at the 76th Scientific Sessions of the American Heart Association; 9-12 November, 2003;
`Orlando, FL, USA.
`
`Sasiela WJ, Szarek M, Silbershatz H, Palmer G. An examination of atorvastatin safety when
`used in combination with amiodarone: evidence from 44 completed clinical trials. Poster
`presentation at the 13 1
`h International Symposium on Atherosclerosis; September 28-0ctober 02,
`2003; Kyoto, Japan.
`
`Sasiela WJ, Szarek M, Silbershatz H, Palmer G. An Examination of Atorvastatin Safety When
`Used in Combination with Verapamil- Evidence from 44 Completed Clinical Trials. Poster
`presentation at the 52nd Scientific Sessions of the American College of Cardiology; 30 March-02
`April, 2003; Chicago, USA.
`
`Engel, SM, Sasiela, WJ, Maggs, DG. Sulfonylurea failure in type 2 diabetics: successful early
`addition of troglitazone in hyperglycemic patients on a half-maximal sulfonylurea dosing.
`Diabetes. 49 (Suppl1):A89, 2000.
`
`Hirsch, IB, Sasiela, WJ, Thompson, RG, Maggs, DG. Treat to target efficacy oftroglitazone
`added to insulin in type 2 diabetes patients in endocrine and primary care practice settings.
`Diabetes. 49 (Suppl 1 ):A90, 2000.
`
`Engel, SM, Miles, JM, Sasiela, WJ, Thompson, RG and Maggs, DG. Succesful early addition of
`troglitazone to half-maximal sulfonylurea in type 2 diabetes: a rationale for earlier use in
`sulfonylurea patients. American Academy of Clinical Endocrinologists, May 2000.
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`CFAD Ex. 1010 (10 of 11)
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`Hirsch, IB, Einhorn, D, Sasiela, WJ, Thompson, RG, Maggs, DG. Efficacy in treatment to
`target: combination of troglitazone and insulin in type 2 diabetes patients in an endocrine
`practice setting .. American Academy of Clinical Endocrinologists, May 2000.
`
`Nachtigal, M., Legrand,A., Sasiela, WJ, Watson, S. and Fowler S.D. Gene expression in
`macrophage foam cells of carrageenan-induced granulomas in hypercholesterolemic rabbits.
`FASEB. J. 6:A454, 1994.
`
`Sasiela, WJ, Hoffman, M., Nachtigal, M. and Fowler S.D. Biological properties of macrophage(cid:173)
`derived foam cells. FASEB J., 7:A792, 1993.
`
`Copley, S.D., Frank, E., Koch, T.H., Kirsch W.M., Hunsaker, R., Van Buskirk, J., Nehlsen(cid:173)
`Cannarella, S., Gasque-Carter, P.D., Sasiela, WJ and Fowler, S.D. Aminomalonic acid (AMA)
`detected in selected proeins from granuloma foam cells by gas chromatography/mass
`spectrometry. FASEB J. 5:A533, 1991.
`
`Koch, T.H., Wheelan, P., Copley, S.D., Wellerson,Jr., R., Kirsch, W.M., Hunsaker, R., Nehlsen(cid:173)
`Cannarella, S., Shi, T.-M., Sasiela, WJ, Gasque-Carter, P.D., and Fowler, S.D. Isolation and
`characterization of aminomalonic acid (AMA) enriched proteins from granuloma cells. F ASEB
`J. 5:A533, 1991.
`
`Kirsch, W.M., Hunsaker, R., Van Buskirk, J., Nehlsen-Cannarella, S., Koln, W., Grinde, S.,
`Gilley, J., Kelin, W., Koch, T.H., Frank, E., Copley, S.D., Sasiela, WJ, Gasque-Carter, P.D. and
`Fowler, S.D. Isolation and characterization of aminomalonic acid (AMA) enriched proteins
`from granuloma cells. FASEB. J. 5:A533, 1991.
`
`Fowler, S.D., Price, R.L., Sullivan, T., Gasque-Carter, P.D., Sasiela, WJ, Copley, S.D., Frank,
`E., Koch, T.H., Hunsaker, R., Nehlsen-Cannarella, S. and Kirsch, W.M. Localization of
`aminomalonic acid (AMA) epitope in granuloma foam cells. FASEB. J. 5:A533, 1991.
`
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