c py
`
`PATENT
`Attorney Docket No. AGP-002
`
`IN THE UNITED STATES PATENT AND TRADEl'.rJARK OFFICE
`
`---······--·----------------·-.......,,.---.......,,.-----------
`In re Patent Application of: Rader
`
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`ppm~atJOn 1 o.:
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`10'-')1 9'1"
`t)~ ,
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`
`Filed: June 21, 2007
`
`For: Methods for Treating Disorders or Diseases
`Associated -~~j-~_h_E!XP.~~!~!p_i_d_el_r_,i._~l ______ _
`
`Confirmation No.:5393
`
`r\rt Unit: 1614
`
`Examiner: K. Weddington
`
`DECLAR.4110N OF ~VILLIAivl SASIELA, PH.D._, UNDb"R 37 CFR 1.132
`
`I, 'WilHam Sasiela, hereby declare as follows:
`
`1, I am Executive Vice President and Chief Medical Ofticer at Aegerion Pharmm.;euticais, 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 rny curriculum vitae attached as Exhibit A.
`
`3. I have read and understood the Application, including the eunently-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 hyperlipiderrda or
`hypercholesterolemia that includes stepwise increasing dose levels, the claimed MTP
`inhibitor had been the subject of human 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 ( ele·vation 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 vvorld's largest category of lipid lowering drugs,
`have not employed, to my lmowledge, step wise increasing doses (titration) in order to
`minimize side effects that would otherv,rise be observed at high doses. Ezetimibe (Zetia®),
`another type of lipid lowering drug, was developed and received FDA approval at a single
`dose level.
`
`CFAD Ex. 1010 (1 of 11)
`
`

`
`7. I believe that the claimed method for treating hyperlipidemia or hypercholesterolernia that
`includes stepwise increasing dose levels as recited in daim 1 would have not been obvious to
`a person skilled in the art at the time ofthe 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 tria! did not a.nive at a solution to the
`adverse events shown in patients at constant level dosing.
`
`8.
`
`Iv1y colleagues and I have supervised Phase I, II, and Ill clinical trials, including Phase II
`randornized, double-blind human clinical trials, to assess the effectiveness and rate of adverse
`events ofthe instantly claimed methods of treating hyperlipidemia or hypercholesterolemia.
`I present belo\V a summary of findings obtained using the claimed method.
`
`9. Patients were administered low doses of the claimed MTP in,.~ibitor (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 arms,
`2A, and 2B, were first administered 5 mg ofthe MTP inhibitor for 4 weeks, then
`adrninistered 7.5 mg of the MTP inhibitor tor 4 weeks, and then administered 10 mg of the
`MTP inhibitor for 4 more weeks. The results are depicted in Table A:
`
`,-·-·-·-···-··--················-------.--, -····---,..·················---········· ·················-········· ··--·····-·-··-·1
`! Rate of G!
`· Discontinuations
`
`Rate of
`Diarrhea
`
`:
`!
`i
`I
`!
`
`Study
`(Total N)
`
`Study
`
`1.
`
`1
`
`Rate of G!
`Study
`adverse
`: Duration
`I
`even~
`!-----+-----·-··+~ l
`"' -
`23/35
`30/35
`9/35
` J.2 vve,.ks
`1 (260)
`10 mg
`!------+-------+------+--····-··---+--- (85.7%)
`(65.7%)
`11/28
`2.A (85)
`. 5~10 mg
`12 weeks
`2/28
`18/28
`!_ ...................... .1 ... ·-··················--,....,.........-----····· ---············---+--_{§43_~_)- _...\_~9.3%)
`I 2B (85)
`li 5~10 mg +
`12 weeks
`1/28
`12/28
`10/28
`!
`10 mg eze
`(42.9%)
`(35.7%)
`! 3 {25)** ! 5-760 mg
`78 vveeks
`12/21
`9/2.1
`I (57.1%)
`L ____________________ i
`···-·--------·--··················-·············
`{42.9%}
`*"'Adverse event rates based on analysts of21 treated patients
`Table A
`
`3/25
`
`I 0. Patients in study 2A had a dramatic difference in the rate of patient discontinuation rate due
`to gastrointestinal (GI) efteets, and in the rate of GI adverse events and dianhea, as compared
`to study 1.
`
`ll. 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 l 0 mg of the Iv1TP inhibitor for 4 more weeks. These patients vvere additionally
`administered ezetimibe (1 0 mg daily, at a eonstant dosage level). Surprisingly, patients
`administered both ezetimihe and the claimed MTP inl1ibitor, 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 rng of the MTP inhibitor alone.
`
`2
`
`CFAD Ex. 1010 (2 of 11)
`
`

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`12. Patients in study 3 suffer from homozygous familial hypercholesterolemia (hoFH), <:J.nd were
`first administered 5 mg of the same MTP inhibitor used in study 1 and 2 for four \:Y'eeks, then
`administered 10 mg of the MTP inhibitor f()r four weeks, then administered 20 mg of the
`MTP inhibitor for four weeks, then 40 mg ofthe MTP inhibitor for four weeks, then 60 mg
`ofthe MTP inhibitor, or to the highest tolerated dose.
`
`13. Surprisingly, the patients in study 3, initially administered 5 mg o,fAfFP inhibitor, and
`subsequently administered up to 60 mg of the MTP inhibitor, after escalation of dose levels
`to a mean dose level of 44 tng/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 redueed 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 '.vithout escalating doses.
`
`15. I hereby declare that all statements made herein of my own knowledge are tme and that all
`statements made on infonnation and belief are believed to be true; and further that these
`statements wen.~ made vvith 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 .
`. /\
`~yL .9-. ....
`
`Dated: April j_, 2010
`
`......... .._R~~~~~~~~~-~-~-~--
`William Sa .el·, Ph.D.
`
`3
`
`CFAD Ex. 1010 (3 of 11)
`
`

`
`"VILLIAJ\1 J. SASlELA, PH.D.
`124 Saxon Way
`Skillman, NJ 08558
`(609)651-3773
`h~asiela(W,aoLcorn
`
`• --.,-.-.·.·.·.·.·.·.·.·.w::::::::::::::."=======··~:.·.·.·.·.·.·.·.·.·.·.·.·.·.·:::::::::::::::."=· ====="'7-·-·.·.·.·.·.·.·.·.·.·.·.·:.w::::::::::======·· ··.·.·.-.,-.-.·.·.·.·.·.·.·.·.·.·.·.·.·.·.·.·.
`
`l~XECUTIVE PRO.FILE
`
`Strong Phase Il-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--lV 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.
`
`PRO_F}~SSIONAL EXPKRIENCE
`
`2005-Present
`
`Aegerion Pharmaceuticals, Inc., Bridgewater, NJ
`Executive Vice President & ChiefM.edical 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 pharmaeokinetic 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 persmmel to support ali 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 tearn with participation and presentation at all
`Aegerion Board of Director meetings.
`• Significant role in all private and public tl.nancing 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.
`
`CFAD Ex. 1010 (4 of 11)
`
`

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`Pfizer/Parke-Davis, New York, NY/Morris Plains, NJ
`
`1996-2005
`
`2003-2005
`Senior Clinical DirectorlfVorldwide Team Leader
`Led Worldvvide l'v1edical Teams for Lipitor and the Atherosclerosis Development at Pfizer's NY
`headqua1iers. 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
`conm1ercialization.
`• 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.
`411 Ensured alignment and appropriate roll-out of medica! strategies betvveen NYHQ, US and
`other key regions.
`411 Played integral role in the development of the extensive phase 3 program and proposed
`labeling f()r torcetrapib/atorvastat1n
`it Led eflorts around lifecycle management for an established product (Lipitor) and an
`emerging product (torcetrapib/atorvastatin)
`• Worked with Pfizer L&D team to identifY and evaluate potential in-licensing candidates.
`Performed technical due diligence on compounds of interest.
`411 Contr1buted to overall PFE strategy in CVJVIE through activity in Therapeutic Area
`Strategy Tearns. In particular, led efforts around identifkation and prioritization of
`enabling strategies for all CVIv1E development areas.
`411 Led a cross-functional team to develop strategies for validation of atherosclerosis
`imaging techniques and plasma biomarkers.
`it Managed multimillion dollar annual budgets for both the Lipitor and Atherosclerosis
`Development programs.
`
`Clinical Director/Lipitor Medical Team
`2000-2003
`i\s a member of the Lipitor Medical Team, directly oversaw key clinical trials and medical(cid:173)
`marketing strategy activities as well as contr1buted to the overall medical and marketing
`strategies for the brand.
`" Directly managed a number of phase IIIb/IV trials such as MIRACL, REVERSAL,
`BELLES and SPARCL 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 eflects of statins.
`
`CFAD Ex. 1010 (5 of 11)
`
`

`
`•
`
`• Led the organization and rnanagement of the 2002 Atorvastatin Global Investigators
`Meeting (1 000+ Global OL attendees)
`Initiated, developed and managed a global research awards prograrn 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.
`411 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 prest~ntations to large managed care and governmental
`organizations
`
`411
`
`1998-2000
`1~1edical Liaison Specialist
`In addition to maintaining regional field medica! 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/trogiitazone betvveen the
`Parke-Davis HQ teams and the US medical liaison tearn.
`" 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 rnedical 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
`troglitaz.one.
`Involvement in national CME programs related to diabetes.
`
`1111
`
`iY!edical Liaison//}r. Medical Liaison
`1996-1998
`i\ member of the first group of medical liaisons at Parke-Davis. At various times covered some
`or all ofthe 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 \vhich 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 H-IV research sites for I1Q medical teams.
`
`•
`
`CFAD Ex. 1010 (6 of 11)
`
`

`
`~ 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.
`to Provide therapeutic area and product training and support to the local sales
`representatives and managers.
`
`-··~.,-~.·-·.·.·.·.·.·.·.·.·.·.·~.-:;~~~~~~~~~~~~~~~-'======'"'"·"·"·"·"·"·"·"·"·"·"·"~.-~.·~~~~~~~~~~~~~-·=====•••-·~-~-·.·.·.·.·.·.·.·.·.·.·.·.·.·.·.•~.·.·~~~~~~~~~~~~~~-~-~ · · - -
`
`POST-DOCTORAL EDtTCATION AND EXPERIENCE
`
`High School Science Instructor- South em Vance High Sd1ool, Henderson, NC. 1995·-1996.
`Taught Physical Science, Biology and Anatomy and Phys·iology
`Voted Best Lecturer by the student body.
`
`]>ost-Doctoral Fellowship- University of North Carolina School of Medicine, Chapel Hill,
`NC. 1994-1995.
`Kathy Pryzvvansky, Advisor
`Research project focused on the role of cGMP and its main intracellular receptor, cGiv1P(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-DOCTOR.A.L EDVCA TION
`
`Ph.D. - Univt~rsity of South Carolina School of Medicine, Columbia, South Carolina
`Experimental Pathology, 1994. Stanley F'o-vvler, Advisor.
`Research into the biological role that macrophage-derived foam cells play in the initiation and
`progression of atherosderotic lesions.
`
`B.S.- Virginia l'olytechnic Institute and State University, Blacksburg, Virginia
`Biochemistry (lllinors in Biology and ChemistrJ), 1987.
`
`Papers and/or l~haptcrs:
`
`PUHLICA1'IONS
`
`Samaha F, McKenney J, Bloedon L, Sasida VV, and Rader, D. Inhibition of Microsomal
`Triglyceride Transfer Protein i\lone or in Co.mbination with Ezetimibe in Patients with Moderate
`I-lypercholesterolemia. Nature Clin Prac Cardiovasc Med. 2008 Aug;5(8):497-505.
`
`CFAD Ex. 1010 (7 of 11)
`
`

`
`Libby P, SasieJa \V. 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~ WJ. Relation of characteristics of metabolic
`syndrome to short-terrn 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., Sasida W.J. An association study of 43 SNPs in 16
`candidate genes with atorvastatin response.
`Phannacogenomics J. 2005;5(6):352-8.
`
`Olsson AG, Schwartz GG, Szarek M, Sasiela '\VJ, Ezekowitz J'v1D, Ganz P, Oliver MF, \Vater 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 '\VJ, Tsai J, Orazem J, Magorien RD,
`O'Shaughnessy C, Ganz P; Reversal of Atherosclerosis with Aggressive Lipid LO\:vering
`(REVERSAL) Investigators. Statin therapy, LDL cholesterol, C-reactive protein, and coronary
`a1tery 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;
`Iv1yocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) Study
`Investigators. High-dose atorvastatin reduces total plasma levels of oxidized phospholipids and
`immune cornplexes present on apolipoprotein B-1 00 in patients \vith 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 (MIRi\CL) Study. Circulation. 2004 Jul
`27;110(4):386-91. Epub 2004 Jul 19.
`
`Kinlay S, Schwartz GG, Olsson A .. G, Rifai N, Leslle 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)
`
`

`
`Fowler, S.D., Gasque-Carter, PJ)., Patillo-Adkisson,E., Sasicla, WJ and
`Xenachis, D.N. Cellular models of atherosclerosis in the young. Chapter 5:
`HyperlipideJ:nia in Childhood and the Developrnent of Atherosclerosis.
`Ann. N.Y.Acad. Sci.,623:60-69, 1991.
`
`Abstracts and presentations:
`
`Bilheimer J, Crowley D, Sasiela \V, 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, Sasida \VJ, Rader D. Efficacy and Safety ofthe MTP(cid:173)
`Inhibitor, AEGR-733, as immunotherapy and in Cornbination with Ezetimibe. Presentation at
`the XVI International Symposium on Drugs Affecting Lipid Metabolism; October 4--7, 2007;
`Nnv York, NY, USA
`
`Samaha F, McKenney J, Bloedon L, Sasiela \VJ, 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, Sasicla \VJ, 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 XV I 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, Sasida \VJ, Rader D, Cuchel M. Impact of
`the l'v1TP 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, Sasicla \VJ, Rader Dl Efficacy and Safety of the I'vfTP(cid:173)
`inbibitor, AEGR-733, as Monotherapy and in Combination with Ezetimibe. Circulation.
`2006;114:U_289.
`
`Schwartz GG, Olsson AG, Chaitman B, Goldberger J, Szarek M, Sasiela W.l Effect of Intensive
`Statin Treatment on the Occurrence of Atrial Fibrillation after Acute Coronary Syndrorne: 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.
`
`Sasicla \VJ, Silbershatz lJ, 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
`
`CFAD Ex. 1010 (9 of 11)
`
`

`
`European Atherosclerosis Society; Apri117-20, 2004; Seville, Spain.
`
`Sasiela WJ, Silbershatz H, Ma J, Villagio E. Effect ofAtorvastatin on Lipoprotein Subfraction
`Profiles in Patients with Dyslipidemia. Poster presentation at the 74th Congress of the European
`Atherosclerosis Society; April17-20, 2004; Seville, Spain.
`
`Sasiela WJ, Silbershatz H, Szarek M. Analysis ofthe 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, Sasicla WJ, Szarek M, Olsson AG, Schwmiz GO.
`Circulating Oxidized LDL Markers Reflect the Clinical Benefit Noted with Atorvastatin in the
`Myocardial Ischemia Reduction with Aggressive Lipid L,owering 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, Sasicla \VJ, 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 Novernber, 2003;
`Orlar1do, FL, USA.
`
`Sasiela 'W,J, 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 13th International Symposimn on Atherosclerosis; September 28-0ctober 02,
`2003; Kyoto, Japan.
`
`Sasiela '\VJ, Szarek M, Silbershatz H, Palmer G. An Examination ofAtorvastatin Safety When
`Used in Combination with Verapamil -- Evidence from 44 Completed Clinical Trials. Poster
`presentation at the 52nd Scientific Sessions ofthe American College of Cardiology; 30 March-02
`April, 2003; Chicago, USA.
`
`Engel, SM, Sasiela, \V~r, Maggs, DG. Sulfonylurea failure in type 2 diabetics: successful early
`addition of troglitazone in hyperglycernic patients on a half-maximal sulfOnylurea dosing.
`Diabetes. 49 (Suppll):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 ):i\90, 2000.
`
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