AstraZeneca Results Presentation Deck

Rare Disease - R&D highlights Accelerating in ALXN2220 to Phase III for ATTR-CM ALXN2220 (NI006) | mAb IgG1 Phase Ib¹ in ATTR-CM CEO Opening Remarks H/WB ratio Total N1006 clearance of cardiac amyloid shown at 4 and 12 months Representative images from scintigraphy after treatment with ALXN2220 A Patient 1, 75yo male, ATTRwt, 60 mg/kg N1006 Baseline 6.9% 4 months 2.5% 20.7 g (46.1 d* mg/ml) Financial Results NI006 improvement in cardiac function (NT-proBNP) ESC European Society of Cardiology + 12 months 2.5% 61.7 g (162.7 d*mg/mL) EDICINE 1551 2010 1856 potential monthly i.v. dosing Selectively binds and removes misfolded amyloid fibrils Oncology 1 2 3 BioPharmaceuticals pathophysiology Complimentary mechanisms transforming ATTR-CM TTR production in the liver Tetramer formation Organ deposition Rare Disease ПО ∞ CEO Closing Remarks 1. Garcia-Pavia et al. NEJM Phase 1 Trial of Antibody ALXN2220 (N1006) for Depletion of Cardiac Transthyretin Amyloid. Representative images from serial bisphosphonate scintigraphy from one patient randomly assigned to receive ALXN2220 (N1006). 2. Alexion, AstraZeneca Rare Disease has the Japanese rights to acoramidis. ATTR-CM = transthyretin amyloid cardiomyopathy; mAb = monoclonal antibody; IgG1 = immunoglobulin G1; yo = year-old; wt = wild- 26 type; H/WB = heart-to-whole body ratio; TTR = transthyretin. Collaboration partner: Neurimmune; lonis; Bridge Bio. medicine and modality Silencer eplontersen blocks TTR synthesis Stabiliser acoramidis² stabilises TTR tetramers Depleter ALXN2220 binds to misfolded TTR, removes toxic fibrils

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