Alnylam Pharmaceuticals, Inc. · NASDAQ:ALNY

Alnylam Pharmaceuticals — ERA-EDTA 2020

24 slides from Alnylam Pharmaceuticals's conference presentation, Jun 7, 2020

  1. Slide 1: ILLUMINATE-A, a Phase 3 Study of Lumasiran in Children and Adults with PH1

    ILLUMINATE-A, a Phase 3 Study of Lumasiran, an Investigational RNAi Therapeutic, in Children and Adults with Primary Hyperoxaluria Type 1 (PH1) Sander F. Garrelfs1,Yaacov Frishberg2, Sally A. Hulton3, Michael J. Koren4, William D. O’Riordan5, Pierre Cochat6, Georges Deschenes7, Hadas Shasha-Lavsky8,

  2. Slide 2: Primary Hyperoxaluria Type 1

    Primary Hyperoxaluria Type 1 Progressive disease mediated by hepatic overproduction of oxalate AGXT Homozygous or compound Excess oxalate results in insoluble As renal function declines In advanced disease, heterozygous AGXT calcium oxalate crystals, leading due to progressive disease, patients mani

  3. Slide 3: Lumasiran: Investigational RNAi therapeutic for PH1

    Lumasiran Investigational RNAi therapeutic for PH1 Defect in PH1 • RNAi is a natural pathway involved in regulation Peroxisome Cytosol of gene expression by targeting mRNA1 Pyruvate Alanine Glycolate • Lumasiran targets the mRNA for HAO1, which GO encodes GO in the liver1 AGT Glyoxylate Glyoxylate G

  4. Slide 4: Lumasiran Clinical Development

    Lumasiran Clinical Development Clinical pharmacology study Efficacy and safety studies in patients with PH1 Phase 1/2 Phase 3 STUDY 001 ILLUMINATE-A ILLUMINATE-B ILLUMINATE-C Healthy volunteers PH1 patients PH1 patients PH1 patients PH1 patients Part A: single ascending Part B: multiple ascending Do

  5. Slide 5: Urinary Oxalate Assays Used in Clinical Trials of Lumasiran

    Urinary Oxalate Assays Used in Clinical Trials of Lumasiran • Enzymatic assay used in the Phase 1/2 study 24 hr urinary oxalate corrected for BSA (mmol/24 hr/1.73m2) (samples from Phase 1/2 and Phase 2 studies of lumasiran) – Used clinically for diagnosis and clinical management – Available at multi

  6. Slide 6: ILLUMINATE-A Phase 3 Study Design

    ILLUMINATE-A Phase 3 Study Design 6-MONTH DOUBLE-BLIND PATIENT POPULATION (N=39) 54-MONTH EXTENSION PERIOD TREATMENT PERIOD Lumasiran • Adults and children ≥6 years 2:1 RANDOMIZATION qM × 3 loading dose, • Urinary oxalate excretion then q3Ma 3.0 mg/kg subcutaneously Lumasiran ≥0.7 mmol/24 hr/1.73 m2

  7. Slide 7: Patient Disposition

    Patient Disposition 39 Randomized 13 Placebo 26 Lumasiran 2 Discontinued lumasiran 1 Withdrew consent 1 Had adverse event 13 Completed 25 Completed • 1 patient discontinued study drug after receiving 1 dose and subsequently withdrew from study 6-month double-blind 6-month double-blind due to inabili

  8. Slide 8: ILLUMINATE-A: Baseline Demographic Characteristics

    ILLUMINATE-A: Baseline Demographic Characteristics Balanced between placebo and lumasiran groups Placebo Lumasiran Overall Demographic characteristic (N=13) (N=26) (N=39) Mean age at informed consent, years (range) 17.0 (6–60) 18.7 (6–47) 18.1 (6–60) Pediatric (0–18 years), n (%) 8 (61.5) 14 (53.8)

  9. Slide 9: ILLUMINATE-A: Baseline Clinical Characteristics

    ILLUMINATE-A: Baseline Clinical Characteristics Balanced between placebo and lumasiran groups Placebo Lumasiran Overall Clinical characteristic (N=13) (N=26) (N=39) Mean 24 hr urinary oxalate excretion corrected for BSAa (SD), mmol/24 hr/1.73 m2 1.79 ± 0.68 1.84 ± 0.60 1.82 ± 0.62 Mean 24 hr urinary

  10. Slide 10: Primary and Secondary Endpoints

    Primary and Secondary Endpoints ILLUMINATE-A met its primary endpoint and all tested secondary endpoints Placebo Lumasiran Difference, Endpoint p-value (N=13) (N=26) Lumasiran−Placebo Primary endpoint Percent change in 24 hr urinary oxalate excretion corrected for –11.8 –65.4 –53.5 1.7 × 10–14 BSA f

  11. Slide 11: Primary Endpoint: Percent Change in 24 hr Urinary Oxalate to Month 6

    Primary Endpoint: Percent Change in 24 hr Urinary Oxalate from Baseline to Month 6 Rapid and sustained reduction in 24 hr urinary oxalate levels Percent change from baseline in 24 hr 20 LS mean average of M3–M6 urinary oxalate corrected for BSA 0 −20 −11.8% Placebo (N=13) −40 −60 −65.4% Lumasiran (N

  12. Slide 12: Subgroup Analysis: Percent Change in 24 hr Urinary Oxalate

    Subgroup Analysis: Percent Change in 24 hr Urinary Oxalate from Baseline to Month 6 Consistent treatment effect across all subgroups, including baseline 24 hr urinary oxalate excretion, pyridoxine use, and eGFR Subgroup Lumasiran–Placebo Overall (n=39) Age at screening 6 to <12 years (n=16) 12 to <1

  13. Slide 13: Secondary Endpoint: Absolute Change in 24 hr Urinary Oxalate

    Secondary Endpoint: Absolute Change in 24 hr Urinary Oxalate Levels from Baseline to Month 6 Rapid and sustained reduction in 24 hr urinary oxalate levels 2.5 24 hr urinary oxalate corrected for LS mean average of M3–M6 (mmol/24 hr/1.73 m2) BSA (mmol/24 hr/1.73 m2) 2.0 1.5 −0.27 Placebo (N=13) 1.0 0

  14. Slide 14: Secondary Endpoint: Percent Change in Urinary Oxalate:Creatinine Ratio

    Secondary Endpoint: Percent Change in 24 hr Urinary Oxalate:Creatinine Ratio from Baseline to Month 6 Rapid and sustained reduction in 24 hr urinary oxalate:creatinine ratio 40 24 hr urinary oxalate:creatinine ratio Percent change from baseline in LS mean average of M3–M6 20 0 −10.8% Placebo (N=13)

  15. Slide 15: Proportion of Patients with Urinary Oxalate ≤1.5 × ULN or ≤ULN

    Secondary Endpoints: Proportion of Patients with 24 hr Urinary Oxalate Level ≤1.5 × ULN or ≤ULN at Month 6 Majority of patients achieved near normalization (≤1.5 × ULN) or normalization (≤ULN) in 24 hr urinary oxalate levels at month 6 p=8.3 × 10–7 100 84% p=0.0010 Lumasiran Patients (%) 52% Placebo

  16. Slide 16: Secondary Endpoint: Percent Change in Plasma Oxalate

    Secondary Endpoint: Percent Change in Plasma Oxalate from Baseline to Month 6 Rapid and sustained reduction in plasma oxalate levels 60 Percent change from baseline in LS mean average of M3–M6 40 plasma oxalate 20 −0.3% Placebo (N=10) 0 −20 −40 −39.8% Lumasiran (N=23) −60 0 20 40 60 80 100 Study vis

  17. Slide 17: Secondary Endpoint: Absolute Change in Plasma Oxalate

    Secondary Endpoint: Absolute Change in Plasma Oxalate from Baseline to Month 6 Rapid and sustained reduction in plasma oxalate levels 30 LS mean average of M3–M6 (µmol/liter) Plasma oxalate (µmol/liter) 25 20 1.3 Placebo (N=10) 15 10 −7.5 Lumasiran (N=23) 5 0 0 20 40 60 80 100 Study visit BL M1 M2 M

  18. Slide 18: Secondary Endpoint: Change in eGFR from Baseline to Month 6

    Secondary Endpoint: Change in eGFR from Baseline to Month 6 eGFR remained stable from baseline to month 6 100 90 eGFR (mL/min/1.73 m2) Placebo (N=13) 80 70 Lumasiran (N=26) 60 50 0 20 40 60 80 100 Study visit BL W2 M1 M2 M3 M4 M5 M6 Dosing 13 13 12 13 13 12 13 13 Patients (N) 26 24 25 25 25 25 25 25

  19. Slide 19: Exploratory Endpoints: Renal Stone Events and Nephrocalcinosis

    Exploratory Endpoints: Renal Stone Events and Nephrocalcinosis No apparent difference between treatment groups with regard to renal stone events; 3 patients with improvements in nephrocalcinosis Renal stone eventsa Nephrocalcinosisb Placebo Lumasiran Placebo Lumasiran Change from baseline to month 6

  20. Slide 20: Exploratory Endpoint: Change in Plasma Glycolate

    Exploratory Endpoint: Change in Plasma Glycolate from Baseline to Month 6 Plasma glycolate initially increased and then plateaued, consistent with reduction in hepatic GO activity Plasma glycolate (µmol/liter) 250 Lumasiran (N=26) 200 150 Placebo (N=13) 100 50 Study visit BL M1 M2 M3 M4 M5 M6 Dosing

  21. Slide 21: Lumasiran Safety Profile

    Lumasiran Safety Profile • There were no deaths, severe, or serious AEs Placebo Lumasiran Event, n (%) (N=13) (N=26) • All AEs were mild or moderate in severity AEs 9 (69) 22 (85) • Most common related AEs were injection-site AEs occurring in ≥10% of patients in either group reactions Injection-site

  22. Slide 22: Conclusions

    Conclusions • PH1 is a rare devastating disease, with high morbidity and mortality in all age groups • Current management options for PH1 are limited and there is an urgent need for new therapies that can reduce hepatic oxalate production, the key toxic metabolite in PH1 • Substantial reduction in u

  23. Slide 23: Acknowledgments

    Acknowledgments Thank you to the patients, investigators, and study staff who participated in the ILLUMINATE-A study ILLUMINATE-A study collaborators: • Samah Alasrawi • Lili Chan • Theresa Kwon • Pallavi Prasad • Spyridon Arampatzis • Hanh Chu • Kia Lee • Bruno Ranchin • Kenneth Aung-Din • Claire D

  24. Slide 24: Challenge Accepted

    To those who say “impossible, impractical, unrealistic,” we say: CHALLENGE ACCEPTED 24 © 2020 Alnylam Pharmaceuticals, Inc.

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