Pre-clinical and Clinical Drug-Drug Interaction Update: New Molecular Entities Approved by FDA in Outline

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1 Pre-clinical and Clinical Drug-Drug Interaction Update: New Molecular Entities Approved by FDA in 2014 Jingjing Yu, M.D., Ph.D Project Manager Drug Interaction Database (DIDB) Program Dept. of Pharmaceutics University of Washington June 29 th, 2015 Outline Scope of the evaluation 2014 New Drug Applications and Biologic License Applications(NDAs/BLAs) highlights: Overview and represented therapeutic classes Drug-drug interaction (DDI) studies involving metabolism, enzyme inhibition and induction DDI studies involving transport mechanism and inhibition Clinically significant DDIs Physiologically based pharmacokinetic (PBPK) modeling and simulation examples Pharmacogenetic (PGx) studies Hepatic/Renal impairment (HI/RI) studies Food effect studies Overall conclusions 2 1

NDAs/BLAs: 2000-2014 NDAs BLAs 30 33 33 24 30 17 21 22 18 16 21 20 15 24 25 5 6 6 6

2012 2013 2014 3 Datasets Used for the Analysis - Metabolism and Transport Drug

available at Drugs@FDA http://www.accessdata.fda.

2 NDAs/BLAs: NDAs BLAs Datasets Used for the Analysis - Metabolism and Transport Drug Interaction Database, University of Washington: data extracted from NDA/BLA Reviews available at Drugs@FDA Access to in vitro and in vivo DDI data 4 2

Therapeutic classes of NMEs in 2014 (n = 41) 5% 5% 5%3% 2% Anti-Infective Agents (12) 29% Oncology (8) Metabolism disorder/endocrinology (7) 7% Gastroenterology (3) Pulmonary (3) 7% 17% 20%

3 Therapeutic classes of NMEs in 2014 (n = 41) 5% 5% 5%3% 2% Anti-Infective Agents (12) 29% Oncology (8) Metabolism disorder/endocrinology (7) 7% Gastroenterology (3) Pulmonary (3) 7% 17% 20% Cardiovascular Drugs (2) Diagnostic Agents (2) Central Nervous System Agents (2) Neurology (1) Skin Agents (1) 17 NMEs (41%) as First-in-Class, indicator of the innovative nature of a drug More orphan drugs for rare diseases (17 NMEs, 41%) than any previous year 5 NDA # Brand Name Drug Name DDI HI/RI Food Effect PGx PBPK Approval Date FARXIGA Dapagliflozin Y Y Y Y N 01/ HETLIOZ Tasimelteon Y Y Y N N 01/ NORTHERA Droxidopa Y N Y N N 02/ NEURACEQ Florbetaben Y (in vitro) N N N N 03/ IMPAVIDO Miltefosine Y N N N N 03/ OTEZLA Apremilast Y Y Y N N 03/ ZYKADIA Ceritinib Y poppk Y N Y 04/ ZONTIVITY Vorapaxar Y Y Y N N 05/ DALVANCE Dalbavancin Y Y N N N 05/ JUBLIA Efinaconazole Y N N N N 06/ SIVEXTRO Tedizolid phosphate Y Y Y N N 06/ BELEODAQ Belinostat Y N N N Y 07/ KERYDIN Tavaborole Y N N N N 07/ ZYDELIG Idelalisib Y Y Y N N 07/ STRIVERDI RESPIMAT Olodaterol Y Y N Y N 07/ JARDIANCE Empagliflozin Y Y Y N N 08/ ORBACTIV Oritavancin Y Y (HI)/popPK(RI) N N N 08/ BELSOMRA Suvorexant Y Y Y N N 08/ CERDELGA Eliglustat Y poppk Y Y Y 08/ MOVANTIK Naloxegol Y Y Y N Y 09/ HARVONI Ledipasvir and sofosbuvir Y Y Y N N 10/ AKYNZEO Netupitant and palonosetron Y Y (HI)/popPK(RI) Y N N 10/ LUMASON Sulfur hexafluoride lipid-type A microspheres Y N N N N 10/ OFEV Nintedanib Y poppk(ri) Y Y N 10/ ESBRIET Pirfenidone Y Y Y N N 10/ XTORO Finafloxacin Y N N N N 12/ ZERBAXA Ceftolozane and tazobactam Y Y (RI) N N N 12/ LYNPARZA Olaparib Y Y (RI) Y N Y 12/ VIEKIRA PAK Ombitasvir, paritaprevir, and ritonavir co-packaged with dasabuvir Y Y Y N N 12/ RAPIVAB Peramivir Y Y (RI) N N N 12/19 3

4 2014 BLAs (n = 11) BLA # Brand Name Drug Name DDI HI/RI Food Effect PGx PBPK Approval Date VIMIZIM Elosulfase alfa N N N N N 02/ MYALEPT Metreleptin N N N N N 02/ TANZEUM Albiglutide Y Y (RI) N N N 04/ CYRAMZA Ramucirumab N N N N N 04/ SYLVANT Siltuximab N N N N N 04/ ENTYVIO Vedolizumab N N N N N 05/ PLEGRIDY Peginterferon beta-1a N N N N N 08/ KEYTRUDA Pembrolizumab N N N N N 09/ TRULICITY Dulaglutide Y Y N N N 09/ BLINCYTO Blinatumomab N N N N Y 12/ OPDIVO Nivolumab N N N N N 12/22 7 Summary of the Studies Assessed in 2014 NDAs/BLAs 30 NDAs + 11 BLAs 30 NDAs + 2 BLAs evaluated further (total of 35NMEs) 9 BLAs No DMPK-transport information available 5 NDAs + 1 BLA PBPK simulations (6 NMEs, 17%) HI/RI data (24 NMEs, 69%) PGx information (4 NMEs, 11%) DDI studies METABOLISM: 35 NMEs TRANSPORT: 25NMEs (71%) Food effect studies (20 NMEs, 57%) 8 4

5 DDI Studies Involving Metabolism, Enzyme Inhibition, and Induction 9 NMEs as Substrates of Enzymes: In vitropositive metabolism (n = 29 NMEs, 83%) 18 Largest # of NMEs metabolized by CYP3A Phase I enzymes Phase II enzymes Number of drugs CYP3A CYP2D6 CYP2C9 CYP2C19 CYP1A2 CYP2C8 CYP2A6 UGTIA1 UGT1A9 CYP1A1 CYP2J2 UGT1A7 UGT1A8 UGT2B4 CYP2B6 CYP2E1 CYP4F UGT1A3 UGT1A4 UGT1A10 SULT1A1 SULT1A3 AO FMO 7 Others 5 Unknown 32 NMEs were evaluated as substrates of specific drug-metabolizing enzymes 14 NMEs were confirmed to be in vivo CYP3A substrates 10 5

NMEs as Substrates of Enzymes: In vivocyp3a inhibition studies (n = 14NMEs, 40%) 14.0 12.0 10.0 12.4 Ketoconazole 200 or 400 mg oral QD or BID 3-28 days Itraconazole 200 mg oral QD for 8 days Max AUC ratio 8.

6 NMEs as Substrates of Enzymes: In vivocyp3a inhibition studies (n = 14NMEs, 40%) Ketoconazole 200 or 400 mg oral QD or BID 3-28 days Itraconazole 200 mg oral QD for 8 days Max AUC ratio *P-gp substrate # BCRP substrate 11 NMEs as Substrates of Enzymes: In vivocyp3a induction studies (n = 14NMEs) Rifampin 600 mg oral QD or BID 5-22 days Carbamazepine 200 mg oral QD or BID for 24 days 0.7 Max AUC ratio All except vorapaxar had labeling impact *P-gp substrate # BCRP substrate 12 6

NMEs as Inhibitors of Enzymes: In vitropositive inhibition (n = 24 NMEs, 69%) Number of drugs 15 10 5 0 15 12 11 9 9 Largest # of NMEs demonstrating CYP3A inhibition 8 6 6 3 3 1 1 1 33 NMEs were

7 NMEs as Inhibitors of Enzymes: In vitropositive inhibition (n = 24 NMEs, 69%) Number of drugs Largest # of NMEs demonstrating CYP3A inhibition NMEs were evaluated as inhibitors of specific drug-metabolizing enzymes 13 NMEs as Inhibitors of Enzymes: In vivo positive inhibition (Max AUCror Cmaxr 1.25, n = 9NMEs) Inhibitor Victim Enzyme AUC Ratio C max Ratio Potency Idelalisib Midazolam CYP3A Strong Netupitant Midazolam CYP3A Moderate Eliglustat* Metoprolol CYP2D Moderate Ombitasvir, Paritasprevir, Dasabuvir (and Ritonavir) Labeling Impact Y (CYP3A substrate) Y (CYP3A substrate) Y (CYP2D6 substrate) Raltegravir UGT1A Moderate N Suvorexant Midazolam CYP3A Weak Y (NTR CYP3A substrate) Brand Name ZYDELIG AKYNZEO CERDELGA VIEKIRA PAK (dosed as combo) BELSOMRA Ledipasvir (and Sofosbuvir) Atazanavir CYP3A Weak N HARVONI (dosed as combo) Oritavancin S-warfarin CYP2C N/A Weak *mechanism-based inhibitor NTR: narrow therapeutic range Y (NTR CYP2C9 substrate) ORBACTIV Ceritinib: inhibitor of CYP2C9 and CYP3A in vitro, R1>1.1, post-marketing requirement for in vivo evaluation 14 7

8 NMEs as Inhibitors of Enzymes: In vitropositive inhibition (n = 24 NMEs, 69%) Number of drugs CYP2C8: a total of 12 inhibitors in vitro, 8 NMEs R1<1.1, 2 NMEs (tasimelteon and vorapxar R1<1.1) in vivo negative (rosiglitazone), 2 NMEs (belinostat and idelalisib) R1>1.1 but not evaluated in vivo CYP2C19: a total of 9 inhibitors in vitro, 6 NMEs R1<1.1, 1 NMEs (oritavancin R1 > 1.1) in vivo negative (omeprazole), 2 NMEs (idelalisib and suvoraxant) R1>1.1 but not evaluated in vivo 15 NMEs as Inducers of Enzymes: in vitro to in vivo translation In vitro, 29 NMEs were evaluated as inducers of specific drugmetabolizing enzymes and 12 NMEs (34%) are identified inducers of at least one of these enzymes, including CYP1A2, 2B6, 2C8, 2C9, 3A4, UGT1A1, UGT1A4, or activators of hpxr; In vivo, only ledipasvir (administered as a combo with sofosbuvir) showed weak induction of CYP2B6 (AUCr = 0.79, Cmaxr = 0.79, substrate efavirenz). 16 8

9 DDI Studies Involving Transport Mechanism and Inhibition 17 NMEs as Substrates of Transporters: In vitropositive studies (n = 16 NMEs, 46%) 15 Largest # of NMEs were shown to be P-gp substrates NMEs were tested in vitro as substrates of specific transporters. 18 9

NMEs as Substrates of Transporters: In vivopossible P-gpinhibition (n = 9NMEs) Ketoconazole 200 or 400 mg oral QD or BID 3-14 days 4.50 4.

10 NMEs as Substrates of Transporters: In vivopossible P-gpinhibition (n = 9NMEs) Ketoconazole 200 or 400 mg oral QD or BID 3-14 days Quinidine 600 mg oral SD Simeprevir 150 mg oral QD for 10 days Max AUC ratio *CYP3A substrate #BCRP substrate ^CYP2C9, CYP2C19, UGT substrate 19 NMEs as Inhibitorsof Transporters: in vitropositive studies (n = 18 NMEs, 51%) Largest # of NMEs were shown to be OATP1B1/3 inhibitors NMEs were tested in vitro as inhibitors of specific transporters

11 Drug Name NMEs as Inhibitorsof Transporters: P-gp: from in vitro(n = 13) to in vivo IC 50 (µm)/ % Inhibition I 1 (µm) I 2 (µm) I 1 /IC 50 I 2 /IC 50 In vivo Victim Apremilast # > < < 5 Nintedanib* 27.1% at 3 µm Olodaterol* # E-08 Pirfenidone 29% at 1000 µm 48.8 Tedizolid* # 15.5% at 60µM 5.9 AUC Ratio I1: mean steady-state total (free and unbound) Cmax following administration of the highest proposed clinical dose. I2: dose of inhibitor (in mol)/250 ml (if IC50 is in a molar unit) I/IC50 values in italic: calculated by the DIDB; *also inhibitor of BCRP in vitro; # also inhibitor of OATP1B1/3 in vitro I1/IC50 cut-off 0.1, I2/IC50 cut-off C max Ratio In vivo studies not needed Dasabuvir* # Digoxin no effect no effect Idelalisib # Digoxin no effect no effect Netupitant* # Efflux ratio reduced from 29 to 4.7 N/A N/A Digoxin no effect no effect Paritaprevir* # Digoxin no effect no effect Eliglustat # Digoxin Suvorexant* # Digoxin Vorapaxar* # Digoxin Ledipasvir* # 46.3% at 1 µm N/A N/A Simeprevir NMEs as Inhibitorsof Transporters: OATP1B1/3: from in vitro(n = 16) to in vivo Drug Name C max (µm) IC 50 (µm) OATP1B1 C max / IC 50 R IC 50 (µm) OATP1B3 C max / IC50 Ceritinib 1.8 >5 < >5 < Dapagliflozin N/A N/A Eliglustat # N/A N/A Ledipasvir* # < <1.25 Olaparib* >100 N/A N/A Suvorexant* # ~ N/A No inhibition R In vivo Victim In vivo Effect In vivo studies not needed Empagliflozin* N/A N/A Simvastatin No effect Idelalisib # N/A N/A Rosuvastatin No effect Dasabuvir* # Paritaprevir* # (dosed as VIEKIRA PAK) Pravastatin Rosuvastatin Cmax/IC50 values in italic: calculated by the DIDB; *also inhibitor of BCRP in vitro; # also inhibitor of P-gp in vitro Cmax/IC50 cut-off 0.1, R cut-off 1.25 Dasabuvir and paritaprevir were administered as combo VIEKIRA PAK with ombitasvir and ritonavir. AUCr: 1.82 Cmaxr: 1.36 AUCr: 2.59 Cmaxr:

12 Drug Name NMEs as Inhibitorsof Transporters: BCRP: from in vitro(n = 11) to in vivo IC 50 (µm) I 1 (µm) I 2 (µm) Empagliflozin # Olodaterol* (inhalation) N/A N/A Vorapaxar* # I 1 /IC 50 I 2 /IC 50 In vivo Effect Suvorexant* # Dasabuvir* # Paritaprevir* # Netupitant* # Tedizolid* # In vivo studies not needed Rosuvastatin AUCr 2.59, Cmaxr7.15 (administered as combo) Follow-up study recommended Post-marketing requirement I1: mean steady-state total (free and unbound) Cmax following administration of the highest proposed clinical dose. I2: dose of inhibitor (in mol)/250 ml (if IC50 is in a molar unit) I/IC50 values in italic: calculated by the DIDB; *also inhibitor of P-gp in vitro; #also inhibitor of OATP1B1/3 in vitro I1/IC50 cut-off 0.1, I2/IC50 cut-off Clinically Significant DDIs: considering both metabolism-and transport-mediated interactions 24 12

13 Clinically Significant Inhibitions (max AUCr or Cmaxr 2): NMEs as Substrates(n = 13 NMEs) Victim Perpetrator Enzymes/ Transporters Max AUC Ratio Max C max Ratio Labeling Impact Reference Paritaprevir Ritonavir CYP3A, P-gp, BCRP, OATPs Y* VIEKIRA PAK Eliglustat Paroxetine CYP2D (EM) 8.20 (EM) Y CERDELGA Ketoconazole CYP3A 4.40 (EM) 4.25 (EM) Y CERDELGA Naloxegol Ketoconazole CYP3A, P-gp Y MOVANTIK Dasabuvir Gemfibrozil CYP2C Y VIEKIRA PAK Tasimelteon Fluvoxamine CYP1A2(3A4, 2C9, 2C19) Y HETLIOZ Pirfenidone Fluvoxamine CYP1A (smokers), 3.97 (non-smokers) 1.78 (smokers), 1.83 (non-smokers) Y ESBRIET Ceritinib Ketoconazole CYP3A Y ZYKADIA Suvorexant Ketoconazole CYP3A Y BELSOMRA Olaparib Itraconazole CYP3A Y LYNPARZA Netupitant Ketoconazole CYP3A N AKYNZEO Ledipasvir Atazanavir/Rit P-gp N HARVONI Droxidopa DDC inhibitors # catecholamine pathway enzymes 2.00 N/A N NORTHERA Vorapaxar Ketoconazole CYP3A N ZONTIVITY *Ritonavir (Rit) is part of the combo drug VIEKIRA PAK used to increase paritaprevirplasma exposure #inhibitors not specified in the NDA Reviews 25 Clinically Significant Inhibitions (max AUCr or Cmaxr 2): NMEs as Inhibitors(n = 7NMEs) Victim Perpetrator Enzyme/ Transporter Max AUC Ratio Max C max Ratio Labeling Impact Reference Midazolam Idelalisib CYP3A Y ZYDELIG Simeprevir Ledipasvir P-gp, (BCRP) N HARVONI Midazolam Netupitant CYP3A Y AKYNZEO Rosuvastatin Ombitasvir, Paritaprevir, Dasabuvir, and Ritonavir OATP1B1/3, BCRP (P, D) Y VIEKIRA PAK Raltegravir UGT1A1 (O, P, D) N VIEKIRA PAK Metoprolol Eliglustat CYP2D (EM) 1.72 (EM) Y CERDELGA 26 13

14 Clinically Significant Inductions (max AUCr or Cmaxr 0.5): NMEs as Substrates (n = 15 NMEs) Enzyme/ Max Max Labeling Victim Perpetrator Reference Transporter AUC Ratio C max Ratio Impact Eliglustat Rifampin CYP3A 0.04 (PM) 0.05 (PM) Y CERDELGA Naloxegol Rifampin CYP3A, P-gp Y MOVANTIK Olaparib Rifampin CYP3A Y LYNPARZA Suvorexant Rifampin CYP3A Y BELSOMRA Tasimelteon Rifampin CYP3A4, 1A2, 2C9, 2C Y HETLIOZ Netupitant Rifampin CYP3A Y AKYNZEO Idelalisib Rifampin CYP3A, P-gp Y ZYDELIG Apremilast Rifampin CYP3A, P-gp Y OTEZLA Ceritinib Rifampin CYP3A Y ZYKADIA Paritaprevir Carbamazepine CYP3A, P-gp Y VIEKIRA PAK Dasabuvir Carbamazepine CYP3A, P-gp Y VIEKIRA PAK Ledipasvir Rifampin P-gp N HARVONI Vorapaxar Rifampin CYP3A N ZONTIVITY Pirfenidone Cigarette smoking CYP1A Y ESBRIET Nintedanib Rifampin CYP3A, P-gp Y OFEV Tasimelteon Cigarette smoking CYP1A (smokers and non-smokers) Y HETLIOZ PBPK Modeling and Simulations 6 NMEs with PBPK simulations: belinostat, blinatumomab, ceritinib, eliglustat, naloxegol, olaparib; 4 NMEs (ceritinib, eliglustat, naloxegol, olaparib) with PBPK results mentioned in the labeling Eliglustat: CYP2D6 and CYP3A metabolism Clinical studies: strong CYP2D6 or CYP3A inhibitors in CYP2D6 EMs PBPK simulations: strong CYP2D6 inhibitor in CYP2D6 IMs moderate CYP2D6 inhibitor in CYP2D6 EM and IMs strong CYP3A inhibitor in CYP2D6 IMs and PMs moderate CYP3A inhibitor in CYP2D6 EMs, IMs and PMs strong CYP2D6 and strong CYP3A inhibitors in CYP2D6 EMs and IMs moderate CYP2D6 and CYP3A inhibitors in CYP2D6 EMs and IMs Alteration in dosage is recommended based on drug interaction studies or on predicted interaction in CYP2D6 EMs, IMs, and PMs

15 Eliglustat Dose Recommendations: EMs and IMs 84 mg orally BID, PMs 84 mg QD 29 Pharmacogenetic Studies 4 NMEs presented some PGx data related to metabolism: eliglustat (CYP2D6), dapagliflozin (UGT1A9), nintedanib (UGT1A1), and olodaterol (UGT1A1/7/9, 2B7). Only eliglustat displayed a significant impact of CYP2D6 polymorphism on its disposition and can be categorized as a sensitive CYP2D6 substrate based on FDA criteria: Since eliglustat has the potential to increase the QT interval, CYP2D6 PM subjects are at risk of cardiac toxicity; while in subjects with UM status, the drug is barely present (90% decrease in exposure) and very likely will not be of any clinical effect; Genotyping CYP2D6 metabolizer status is recommended

Hepatic and Renal Impairment Studies 31 Hepatic Impairment (HI): AUC Ratio 2 vs Normal Controls (n = 4 NMEs) Max AUC Ratio 7 6 5 4 3 2 1 0 Extensive metabolism, 71% fecal (mainly metabolites), 4%

16 Hepatic and Renal Impairment Studies 31 Hepatic Impairment (HI): AUC Ratio 2 vs Normal Controls (n = 4 NMEs) Max AUC Ratio Extensive metabolism, 71% fecal (mainly metabolites), 4% renal 6.1 Sev Extensive metabolism, 88% fecal (mainly metabolites), 9% renal (mainly metabolites) Netupitant Paritaprevir Dasabuvir Tasimelteon All the results have labeling impact. Extensive metabolism, 94% fecal (mainly metabolite), 2% renal 5.3 Sev 3.5 Sev 2.7 Mod Extensive metabolism, 80% renal (mainly metabolites), 4% fecal (mainly parent) not evaluated in severe Moderate HI: Child-Pugh Class B Severe HI: Child-Pugh Class C 16

17 Renal Impairment (RI): AUC Ratio 2 vs Normal Controls (n = 9 NMEs) Max AUC Ratio ESRD 3.2 Mod 2.8 Sev 2.6 Mod 2.3 Sev Peramivir Naloxegol Albiglutide Ceftolozane Dapagliflozin Dalbavancin Tazobactam Apremilast Pirfenidone 2.0 Sev 2.0 Mod M12 (inactive): carboxy (inactive): Sev Sev All the results have labeling impact. minimal metabolism, mainly renal excretion extensive metabolism, mainly biliary excretion extensive metabolism, mainly renal excretion proteolytic degradation Moderate RI: CrCL ml/min Severe RI: CrCL <30 ml/min ESRD: End Stage Renal Disease 33 Food Effect Studies Drug Name AUC Ratio Cmax Ratio Labeling Impact Reference Ceritinib Y (empty) ZYKADIA Dasabuvir Y (food) VIEKIRA PAK Droxidopa Y (either) NORTHERA Naloxegol Y (empty) MOVANTIK Ombitasvir Y (food) VIEKIRA PAK Paritaprevir Y (food) VIEKIRA PAK Pirfenidone Y (food) ESBRIET Tasimelteon Y (empty) HETLIOZ Note: AUC and Cmax ratios vs fasted state 20 NMEs (57%) were studied for food effect with high-, moderate- or low-fat meals

Overall Conclusions Almost all NMEs were extensively studied in vitro, including evaluations of both metabolism and transport; As victims, almost half of the NMEs evaluated had clinically significant

18 Overall Conclusions Almost all NMEs were extensively studied in vitro, including evaluations of both metabolism and transport; As victims, almost half of the NMEs evaluated had clinically significant DDIs, with 6 NMEs considered as sensitive substrates of CYP1A2 (tasimelteon and pirfenidone), 2C8(dasabuvir), 2D6(eliglustat), and 3A(paritaprevir and naloxegol); As perpetrators: 1 NME (idelalisib) was a strong inhibitor of CYP3A 5 NMEs moderately inhibited CYP3A (netupitant), 2D6 (eliglustat), or UGT1A1 (ombitasvir/paritaprevir/dasabuvir dosed as VIEKIRA PAK) 1 NME (ledipasvir) weakly induced CYP2B6 Clinical transporter-based drug interactions : Inhibition of P-gpby moderate inhibitor ledipasvir and weak inhibitors eliglustat, suvorexant, and vorapaxar Paritaprevir/dasabuvir(dosed as VIEKIRA PAK) moderately inhibited OATP1B1/3 and BCRP Organ impairment: 4 NMEs were significantly affected by HI, while 9 were significantly affected by RI. 35 Acknowledgements DIDB Program Team Dr. Isabelle Ragueneau-Majlessi Dr. Nina Isoherranen Dr. Cathy Yeung Dr. Sophie Argon (PGx) Dr. Tasha Ritchie (Transporter) Dr. Zhu Zhou (HI,RI, PBPK) Marjorie Imperial Dr. Katie Owens Dr. Jessica Sontheimer Grace Lee DIDBers! 36 18

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LUNCH AND LEARN. April 10, 2015

LUNCH AND LEARN. April 10, 2015 LUNCH AND LEARN New Drugs 2014 Part 1 April 10, 2015 Featured Speaker: Mary Lynn Moody, RPh Director, Business Development Drug Information Group Clinical Associate Professor University of Illinois at