Dianthus Therapeutics, Inc. · NASDAQ:DNTH

Dianthus Therapeutics — Investor Presentation (January 2026)

74 slides from Dianthus Therapeutics's investor presentation, Jan 12, 2026

  1. Slide 1: Advancing a leading autoimmune-focused company

    Advancing a leading autoimmune-focused company January 2026 Exhibit 99.1

  2. Slide 2: Forward-looking statements

    Forward-looking statements Certain statements in this presentation, other than purely historical information, may constitute “forward-looking statements” within the meaning of the federal securities laws, including for purposes of the safe harbor provisions under the United States Private Securities

  3. Slide 3: Advancing a leading autoimmune-focused company

    Developing two autoimmune therapeutics with best-in-class, pipeline-in-a-product potential and targeting patient-friendly, infrequent S.C. self-administration Advancing a leading autoimmune-focused company Highly potent, ~8-week half-life, classical pathway (CP) inhibitor targeting active C1s Valida

  4. Slide 4: Two clinical-stage candidates with best-in-class, pipeline-in-a-product potential

    Two clinical-stage candidates with best-in-class, pipeline-in-a-product potential Indications Market Insight Our Opportunity Next Milestone gMG: >100,000 gMG U.S. patients from Komodo claims data accessed 2013-2025; approx. 85% of gMG patients have AChR autoantibody-driven disease https://www.ncbi.n

  5. Slide 5: Claseprubart: Building a Best-in-Class Neuromuscular Franchise

    Claseprubart: Building a Best-in-Class Neuromuscular Franchise

  6. Slide 6: Pursuing the power of consistent control…with one-click!

    Pursuing the power of consistent control…with one-click! Targeting a best-in-class, first-line biologic treatment for neuromuscular diseases CLASSICAL CONVENIENCE Upstream Inhibition of Classical Pathway Only <10-Second Autoinjector Targeting No Boxed Warning or REMS Self-Administered At Home or On-

  7. Slide 7: Claseprubart has opportunity to compete as a first-line biologic in large and growing US neuromuscular market

    Claseprubart has opportunity to compete as a first-line biologic in large and growing US neuromuscular market >100K patients >140K patients >150K patients AChR+ gMG patients Positive Ph. 2 data reported Sept. ’25 >40K CIDP patients Ph. 3 interim responder expected in Q2’26 Ph. 2 top-line data expect

  8. Slide 8: Claseprubart: Opportunity to be a Best-in-Class, First-Line Biologic for Generalized Myasthenia Gravis

    Claseprubart: Opportunity to be a Best-in-Class, First-Line Biologic for Generalized Myasthenia Gravis

  9. Slide 9: Ultomiris is the leading blockbuster complement inhibitor, with growth driven by first-line biologic use in gMG

    “Currently, less than 20% of (gMG) patients are on branded treatments, and we expect this to increase to approximately 50% in the next 3 years. Additionally, self-administered medicine represent only a small part of this market today, and we expect this segment to grow substantially.” Ultomiris sale

  10. Slide 10: The multibillion-dollar US gMG market has significant potential to expand

    The multibillion-dollar US gMG market has significant potential to expand as <20% of AChR+ patients1 currently treated with biologics Note: Positioning of claseprubart’s target profile is illustrative. (1) Komodo claims data accessed 2013-2025, adjusted to account for 70% capture of real-world patie

  11. Slide 11: Claseprubart aims to address the significant unmet needs in the gMG market

    Claseprubart aims to address the significant unmet needs in the gMG market Survey of US Neurologists confirms significant opportunity for differentiated biologic in gMG market Dianthus 2025 Neurologist MG quantitative survey (n=81, N = 54 Neuromuscular specialists, N = 27 General Neurologists), fiel

  12. Slide 12: MaGic Ph. 2 Results Support a Potentially Best-in-Class Treatment for gMG

    MaGic Ph. 2 Results Support a Potentially Best-in-Class Treatment for gMG

  13. Slide 13: MaGic Ph. 2 top-line results support a potentially best-in-class treatment for gMG

    MaGic Ph. 2 top-line results support a potentially best-in-class treatment for gMG Strong results support claseprubart potential as a best-in-class complement inhibitor Rapid, sustained, statistically significant symptom improvements as measured by MG-ADL, QMG, MSE, MGC, MG-QoL-15r Safety Endpoints

  14. Slide 14: MaGic is a global Ph. 2 trial in AChR+ gMG patients

    MaGic is a global Ph. 2 trial in AChR+ gMG patients A global, multicenter, randomized, double-blind, placebo-controlled study to evaluate the safety, efficacy, and PK / PD of claseprubart administered S.C. following initial loading dose Trial enrollment exceeded target, with 65 participants enrolled

  15. Slide 15: AChR+ gMG participants baseline characteristics

    AChR+ gMG participants Placebo (N=22) Claseprubart 300mg/2mL Q2W (N=21) Claseprubart 600mg/4mL Q2W (N=22) Age, mean (SD), years 52.2 (16.5) 57.1 (13.7) 55.3 (12.0) Male, n (%) 13 (59%) 14 (67%) 10 (45%) Weight, mean (SD), pounds 195.0 (48.0) 192.5 (35.5) 179.0 (35.4) Duration of disease, median (ran

  16. Slide 16: Statistically significant improvement in MG-ADL score for both claseprubart arms vs. placebo at Week 13

    Statistically significant improvement in MG-ADL score for both claseprubart arms vs. placebo at Week 13 Statistically significant and clinically meaningful reductions in MG-ADL across both treatment arms Mean Change in MG-ADL Score from Baseline at Week 13 The change from baseline in MG-ADL was anal

  17. Slide 17: Statistically significant improvement in QMG score for both claseprubart arms vs. placebo at Week 13

    Statistically significant improvement in QMG score for both claseprubart arms vs. placebo at Week 13 Statistically significant and clinically meaningful reductions in QMG across both treatment arms The change from baseline in QMG was analyzed using a mixed effect model for repeated measures (MMRM) w

  18. Slide 18: Claseprubart arms demonstrated rapid, sustained, and clinically meaningful improvements in MG-ADL score

    -1.8 -2.6 P=0.0113* P=0.0006* Claseprubart arms demonstrated rapid, sustained, and clinically meaningful improvements in MG-ADL score MG-ADL improvements for participants treated with claseprubart were rapid, sustained, clinically meaningful and statistically significant as early as Week 1 The chang

  19. Slide 19: Claseprubart arms demonstrated rapid, sustained, and clinically meaningful improvements in QMG score

    Claseprubart arms demonstrated rapid, sustained, and clinically meaningful improvements in QMG score QMG improvements for participants treated with claseprubart were rapid, sustained, clinically meaningful and statistically significant as early as Week 1 The change from baseline in QMG was analyzed

  20. Slide 20: >60% of participants on claseprubart 300mg/2mL achieved ≥5 point improvement in MG-ADL

    >60% of participants on claseprubart 300mg/2mL achieved ≥5 point improvement in MG-ADL Participants across both treatment arms achieved robust improvements in MG-ADL at Week 13 Improvement in MG-ADL Total Score Claseprubart 300mg/2mL Q2W Placebo Claseprubart 600mg/4mL Q2W Placebo

  21. Slide 21: >60% of participants on claseprubart 300mg/2mL achieved ≥5 point improvement in QMG

    >60% of participants on claseprubart 300mg/2mL achieved ≥5 point improvement in QMG Participants across both treatment arms achieved robust improvements in QMG at Week 13 Improvement in QMG Total Score Claseprubart 300mg/2mL Placebo Claseprubart 600mg/4mL Placebo

  22. Slide 22: 37% of 300mg/2mL participants achieved Minimal Symptom Expression on MG-ADL at Week 13

    37% of 300mg/2mL claseprubart-treated participants achieved Minimal Symptom Expression on MG-ADL at Week 13 MSE supports potential best-in-class profile Minimal Symptom Expression (MSE) % of Participants Achieving MG-ADL Score of 0 or 1 at Week 13 P=0.0550* P=0.1031 The proportion of participants wh

  23. Slide 23: Statistically significant improvement in MGC for both claseprubart arms vs. placebo at Week 13

    Statistically significant improvement in MGC for both claseprubart arms vs. placebo at Week 13 Mean Change in MGC Score from Baseline at Week 13 Mean Change in MGC Summed Muscle Score from Baseline at Week 13 (post-hoc analysis) The change from baseline in MGC and MGC Summed Muscle Score were separa

  24. Slide 24: Statistically significant improvement in MG-QoL-15r score for 300mg/2mL vs. placebo at Week 13

    Statistically significant improvement in MG-QoL-15r score for 300mg/2mL vs. placebo at Week 13 The change from baseline in MG-QoL 15r was analyzed using a general linear model with treatment group, stratification factors, and baseline measure included. *One-sided p-values are presented for compariso

  25. Slide 25: Across key efficacy measures, claseprubart demonstrated robust and clinically meaningful responses

    Across key efficacy measures, claseprubart demonstrated robust and clinically meaningful responses Placebo Claseprubart 300mg/2mL Q2W Claseprubart 600mg/4mL Q2W Absolute Placebo-adjusted Absolute Placebo-adjusted MG-ADL mean change from baseline at Week 13 -2.8 -4.6 -1.8 (P=0.0113)* -5.4 -2.6 (P=0.0

  26. Slide 26: Claseprubart demonstrated statistically significant and clinically meaningful improvements in MG-ADL

    Claseprubart demonstrated statistically significant and clinically meaningful improvements in MG-ADL Claseprubart S.C. Zilbrysq QD PFS Δ1.8 Δ2.6 Note: For illustrative purposes only. Efficacy data are derived from different clinical trials conducted at different times, with differences in trial desi

  27. Slide 27: Additional secondary efficacy measures support claseprubart potential as best-in-class complement inhibitor

    Additional secondary efficacy measures support claseprubart potential as best-in-class complement inhibitor Claseprubart S.C. Ph II MAGIC Week 13 n = 43 | BL = 13.2 Mean Change from Baseline in QMG Score Ultomiris IV Ph III CHAMPION MG Week 26 n = 78 | BL = 14.8 % of Participants Achieving MG-ADL Sc

  28. Slide 28: Claseprubart was generally well tolerated, with a favorable safety profile in Phase 2

    Claseprubart was generally well tolerated, with a favorable, potentially differentiated safety profile in Phase 2 Comparable clinical safety profile to placebo with remarkably benign administration, no infection signal and no symptoms indicative of autoimmune activation Placebo (N=22) Claseprubart 3

  29. Slide 29: Rationale for Q4W 300mg/2mL Dosing & Potential for Enhanced, Best-in-Class Efficacy in gMG

    Rationale for Q4W 300mg/2mL Dosing & Potential for Enhanced, Best-in-Class Efficacy in gMG

  30. Slide 30: OLE data support addition of 300mg/2mL Q4W in Ph. 3

    OLE data support addition of 300mg/2mL Q4W in Ph. 3 Mean Change in PBO Patients’ MG-ADL and QMG Score from RCT Baseline to OLE Week 6 QMG: 14.2 RCT Period OLE Period PBO Patients Entering OLE Received 600mg/4mL Q2W w/ No Loading Dose PK of ~65 µg/mL at week 4 after only two 600mg/4mL doses is substa

  31. Slide 31: Patients with QMG ≥10: adding QMG screening criteria in Ph. 3

    Patients with QMG ≥10 Adding QMG screening criteria in Ph. 3, similar to zilucoplan Ph. 31, may better control for placebo response Claseprubart MG-ADL Change from Baseline P=0.0006* -3.0 P=0.0113* -1.8 The change from baseline in ADL was analyzed using a mixed effect model for repeated measures (MM

  32. Slide 32: Potential for improved efficacy vs. C5 inhibitors may be due to upstream inhibition

    Potential for improved efficacy vs. C5 inhibitors with claseprubart may be due to upstream inhibition Upstream inhibition prevents the creation of pro-inflammatory C3a and C3b as well as MAC, potentially providing additional efficacy benefits for AChR+ gMG patients C3a Formation1 C3b Deposition2* 10

  33. Slide 33: Ph. 3 trial design to include additional Q4W arm and new screening criteria

    Ph. 3 trial design to include additional Q4W arm, and new screening criteria of QMG >10 as well as MG-ADL >6 Potential to further enhance best-in-class differentiation on efficacy and dosing convenience with QMG screening criteria and 300mg/2mL Q4W dosing Final Ph. 3 trial design TBD after regulator

  34. Slide 34: Achieving this profile could position claseprubart as a potential best-in-disease treatment for gMG

    Achieving this profile could position claseprubart as a potential best-in-disease treatment for gMG Similar or superior MG-ADL to FDA-approved C5 inhibitors with continuous, effective symptom control C1s SAFETY (Enjaymo) C5 OR SUPERIOR EFFICACY (ULTOMIRIS/SOLIRIS/ZILBRYSQ) AUTOINJECTOR CONVENIENCE (

  35. Slide 35: Claseprubart: Opportunity to Change the Treatment Paradigm in CIDP

    Claseprubart: Opportunity to Change the Treatment Paradigm in Chronic Inflammatory Demyelinating Polyneuropathy

  36. Slide 36: The US CIDP market offers substantial growth given the high unmet need

    The US CIDP market offers substantial growth given the high unmet need and limitations of the current standard of care Opportunity for an active C1s inhibitor with the target profile of claseprubart to replace the standard of care Current Ig and biologics account for >$3.5B3,4,5 Despite SoC, many (3

  37. Slide 37: Neuromuscular indication with high unmet medical need

    Neuromuscular indication with high unmet medical need Evidence supports classical complement role in disease Active C1s inhibition has demonstrated clinical POC with potential for equal or superior efficacy to current SOC IVIG Claseprubart target dose of 300mg/2mL S.C. every two weeks may offer more

  38. Slide 38: Claseprubart has superior affinity and potency vs. riliprubart

    Claseprubart has superior affinity and potency vs. riliprubart Note: Riliprubart is produced using sequence from patent WO2018071676A1 1. Data shown is dissociation constant (KD) and the average of 3 different experiments performed at independent laboratories 2. Data is quantitative analysis of acti

  39. Slide 39: CIDP Ph. 3 pivotal trial includes open-label Part A testing target dose

    CIDP Ph. 3 pivotal trial includes open-label Part A testing the target dose of 300mg/2mL S.C. Q2W CIDP interim responder analysis with first 40 patients in Part A anticipated in Q2’26 Claseprubart 300mg/2mL S.C. Q2W (N=64) Placebo (N=64) Claseprubart 600mg/4mL S.C. Q2W (N=64) Screen PART A: Up to 13

  40. Slide 40: Key differences between ADHERE and CAPTIVATE trials make cross-trial comparisons challenging

    Key differences between ADHERE and CAPTIVATE trials make cross-trial comparisons challenging Source: Company filings, presentations and clinicaltrials.gov ADHERE required removal of IVIG and evidence of clinically meaningful deterioration before dosing in Part A Defined as a clinical improvement on

  41. Slide 41: Claseprubart: Opportunity to be Best-in-Class in Multifocal Motor Neuropathy

    Claseprubart: Opportunity to be Best-in-Class in Multifocal Motor Neuropathy

  42. Slide 42: The US MMN market is underdiagnosed with a need for more effective and convenient treatment options

    The US MMN market is underdiagnosed with a need for more effective and convenient treatment options US MMN Market Opportunity Opportunity for the target profile of claseprubart to become the new standard of care in MMN 1. 2024 patients projected from 2023 count due to unreliable 2024 data from the C

  43. Slide 43: Neuromuscular indication with high unmet medical need

    Neuromuscular indication with high unmet medical need Evidence supports classical complement role in disease MMN is an attractive opportunity with clinical PoC demonstrated via classical pathway inhibition Phase 2 trial of claseprubart, a low-volume Q2W S.C., ongoing in MMN No approved targeted biol

  44. Slide 44: Claseprubart demonstrates superior classical pathway potency vs. empasiprubart

    Claseprubart demonstrates superior classical pathway potency vs. empasiprubart Claseprubart Demonstrates Superior Classical Pathway Potency Head-to-head vs. Empasiprubart Using Same Assay claseprubart empasiprubart IC50 (µg/mL) 3.8 ± 0.8 22.1 ± 5.7 Empasiprubart Published Classical Pathway Potency D

  45. Slide 45: Key Differentiators of Claseprubart vs. empasiprubart

    Considerations Empasiprubart (C2)* Claseprubart (active C1s)* Key Differentiators of Claseprubart MMN is an IgM and classical pathway driven disease1 Published classical pathway3 EC50 = 30.5 ±4.5 µg/mL using Quidel MicroVue CH50 Claseprubart has demonstrated potent inhibition of classical pathway in

  46. Slide 46: MMN Phase 2 top-line data anticipated 2H'26

    MMN Phase 2 top-line data anticipated 2H’26 A global, multicenter, randomized, double-blind, placebo-controlled study to evaluate the safety, efficacy, and PK / PD of claseprubart administered S.C. following initial loading dose Top-line data expected in 2H’26 MoMeNtum Trial: https://clinicaltrials.

  47. Slide 47: DNTH212: Potential Best-in-Class Bispecific Fusion Protein for Multiple Autoimmune Indications

    DNTH212: Potential Best-in-Class Bispecific Fusion Protein for Multiple Autoimmune Indications

  48. Slide 48: DNTH212 is a bifunctional BDCA2 and BAFF/APRIL inhibitor targeting two validated pathways

    Inhibiting BDCA2 reduces Type 1 interferon production from plasmacytoid dendritic cells (pDCs) Single CRD2 domain of TACI designed to deliver robust B cell modulation via BAFF/APRIL inhibition DNTH212 targets both the innate and adaptive immune systems with complementary disease modifying mechanisms

  49. Slide 49: Potential to drive superior clinical efficacy by targeting both innate and adaptive immune systems

    Potential to drive superior clinical efficacy by targeting both the innate and adaptive immune systems Panda SK, et al., Plasmacytoid dendritic cells in autoimmunity. Curr Opin Immunol. 2017 Feb;44:20-25. Minaga K, et al., Plasmacytoid Dendritic Cells as a New Therapeutic Target for Autoimmune. Fron

  50. Slide 50: DNTH212 achieves superior pDC depletion compared to litifilimab in vitro

    DNTH212 achieves superior pDC depletion compared to litifilimab in vitro Comparable Suppression of Pro-Inflammatory Cytokine IFN-α1 Deeper Depletion of pDC2 Method: Human PBMCs from a healthy donor were co-cultured with a TLR9 agonist and serially diluted antibodies for 24 hours. IFN-α release in th

  51. Slide 51: DNTH212 shows superior inhibition of IgM, IgA, and IgG compared to povetacicept in NHPs

    DNTH212 shows superior inhibition of IgM, IgA, and IgG compared to povetacicept following single dose in NHPs S.C. DNTH212 IV povetacicept and telitacicept1 Note: These data are derived from different studies at different points in time, with differences in methodology, design and populations. As a

  52. Slide 52: Validation of both BDCA2 and BAFF/APRIL targeted therapies support DNTH212 bifunctional approach

    Validation of both BDCA2 and BAFF/APRIL targeted therapies support DNTH212 bifunctional approach Note: Company press releases and investor presentations Positive Litifilimab (BDCA2) Data in SLE / CLE BAFF/APRIL Validation Across Multiple Autoimmune Indications and Strategic Activity

  53. Slide 53: Broad opportunity for DNTH212 across multiple diseases

    Biological Rationale Clinical Evidence Primary Sjögren's Syndrome ~350,000 U.S. Patients  B Cell: ianalumab positive Ph. 3; telitacicept positive Ph. 3 Cutaneous Lupus Erythematosus ~300,000 U.S. Patients  Type 1 interferon: litifilimab positive Ph. 2 Systemic Lupus Erythematosus ~225,000 U.S. Pat

  54. Slide 54: Ph. 1 study initiated in China in Dec. '25 with top-line results in 2H'26

    Ph. 1 study initiated in China in Dec. ’25 with top-line Part A HV results in 2H’26 5mg N = 2:0 S.C. Administration Healthy Volunteers (Part A) ~46 HVs enrolled into seven cohorts: Treated (N= up to 6) Placebo (N= up to 2) ~30 patients enrolled into three cohorts: Treated (N= up to 10) Healthy Volun

  55. Slide 55: DNTH212 TPP aims to deliver superior efficacy in a safe and well-tolerated therapy

    DNTH212 TPP aims to deliver superior efficacy in a safe and well-tolerated therapy with patient friendly convenience Achieving the TPP would position DNTH212 as a first-line biologic across a range of indications Bifunctional approach has potential for superior efficacy in various disease states ver

  56. Slide 56: Achieving DNTH212 TPP would position it as a first-line, best-in-class therapy

    Achieving DNTH212 TPP would position DNTH212 as a first-line, best-in-class therapy across multiple indications Type 1 interferon and BAFF/APRIL are known drivers of autoimmune disease Potential S.C. self-administration Q4W or less frequent Targeting innate and adaptive immune systems has potential

  57. Slide 57: Recap of Dianthus Leadership in Severe Autoimmune Diseases

    Recap of Dianthus Leadership in Severe Autoimmune Diseases

  58. Slide 58: Advancing a leading autoimmune-focused biotech with two clinical-stage programs

    Advancing a leading autoimmune-focused biotech with two-clinical stage programs Program Indication Ph. 1 Ph. 2 Ph. 3 Upcoming Milestones Claseprubart aC1s gMG >100,000 U.S. Patients Expect to initiate Ph. 3 study in 2026 CIDP >40,000 U.S. Patients Interim responder analysis expected in Q2’26 Peer Ca

  59. Slide 59: Appendix

    Appendix

  60. Slide 60: C1s is a clinically validated target in the classical complement pathway

    C1q lgG antibody Cell Surface C1s is a clinically validated target in the classical complement pathway with an FDA approved therapy The C1 complex The initial component of the classical complement pathway consisting of C1q, C1r and C1s 3 2 2 3 Active C1s A serine protease that executes catalytic fun

  61. Slide 61: Selectively targeting classical pathway aims to provide effective but safer complement inhibitor

    Membrane Attack Complex (MAC) Selectively targeting classical pathway aims to provide effective but safer complement inhibitor Targeting aC1s aims to deliver efficacy demonstrated with terminal inhibitors while preserving the critical immune activity of lectin and alternative pathways, leading to a

  62. Slide 62: Unlike C5 inhibitors, ENJAYMO has no FDA boxed warning and REMS

    Unlike C5 inhibitors, ENJAYMO® has no FDA boxed warning and REMS, or prophylactic antibiotic requirement prior to vaccination Source: ULTOMIRIS prescribing information & ENJAYMO prescribing information Boxed Warning and REMS Antibiotic Prophylaxis Required if not Fully Vaccinated No Boxed Warning or

  63. Slide 63: Claseprubart in vitro study indicates lower risk of Neisseria meningitidis infections

    Claseprubart in vitro study indicates lower risk of Neisseria meningitidis infections Anti-capsular antibody (Anti -Nm) mimics N. meningitidis vaccination 0 50 100 150 % Bacterial Survival Serum +Anti - Nm 0.3 uM 1.0 uM DNTH103 Anti - C5 No treatment Results further validate the potential different

  64. Slide 64: Claseprubart aims to provide consistent symptom control with convenient Q2W S.C. dosing

    Indicates VYVGART® dose administered Source: VYVGART® prescribing information and ULTOMIRIS® prescribing information 1. Pane et al. A real-life experience with eculizumab and efgartigimod in generalized myasthenia gravis patients. J Neurol 271, 6209–6219 (2024) Claseprubart aims to provide consisten

  65. Slide 65: Patients on eculizumab showed a greater reduction in MG-ADL over time than those on efgartigimod

    Patients on eculizumab showed a greater reduction in MG-ADL over time than those on efgartigimod Eculizumab showed statistically significant, deeper QMG reduction and higher responder rate than efgartigimod Eculizumab patients had a statistically significant greater reduction in rate of clinical eve

  66. Slide 66: Claseprubart improves neurotransmission and muscle contraction in an AChR+ MG model

    Claseprubart improves neurotransmission and muscle contraction in an AChR+ MG model Results provide further scientific rationale for DNTH103 in gMG Serum from MG patients used in a validated in vitro MG model1,2,3 Assessed improvement in neurotransmission and muscle contraction of ravulizumab* and D

  67. Slide 67: Claseprubart restores neuronal conduction velocity in an in vitro CIDP model

    Claseprubart restores neuronal conduction velocity in an in vitro CIDP model Results provide further scientific rationale for DNTH103 in CIDP Serum from 3 CIDP patients was evaluated in a , commercially available in vitro CIDP model1 Assessed improvement in neuronal conduction velocity of two doses

  68. Slide 68: Claseprubart Phase 1 healthy volunteer study design

    SAD 1 (1 mg/kg) SAD 3 (30 mg/kg) SAD 2 (10 mg/kg) MAD 1 Q2W (300mg/2mL) MAD 2 Q2W (600mg/4mL mg) SAD 1 (300mg/2mL) SAD 2 (600mg/4mL) I.V. Administration S.C. Administration S.C. Administration SAD MAD Claseprubart Phase 1 healthy volunteer study was designed to validate extended half-life, potency a

  69. Slide 69: Claseprubart has demonstrated deep and sustained complement inhibition in healthy volunteers

    Claseprubart has demonstrated deep and sustained complement inhibition in healthy volunteers Claseprubart demonstrated a ~60-day half-life and IC90 of 87 µg/mL I.V. SAD: Linear PK with Exposure Proportional Across Doses S.C. MAD: Strong Accumulation with Q2W Dosing PK/PD: Analysis Demonstrates IC90

  70. Slide 70: Ph. 1 data estimated IC90 at ~87 µg/mL, leading to target dose of 300mg/2mL

    15mg/kg I.V. on Day 0 300mg S.C. Q2W starting Day 7 Phase 1 data estimated IC90 at ~87 µg/mL, leading to target dose of 300mg/2mL in Ph. 2 to achieve steady state >IC90 ~60-day half-life IC90 calculated at 87 µg/mL Ph. 1 Data Confirms Simulation using data from 60 healthy volunteers dosed across mul

  71. Slide 71: Claseprubart was generally well tolerated, with a favorable safety profile in Phase 1

    Claseprubart was generally well tolerated, with a favorable safety profile in Phase 1 No standard safety lab findings (hematology, chemistry, coagulation LFTS and renal function) No serious adverse events No infection adverse event signal and no infections related to encapsulated bacteria Five parti

  72. Slide 72: C3a and C3b Are Elevated in AChR+ gMG

    C3a and C3b Are Elevated in AChR+ gMG – Both Cause Inflammatory Damage1,2 C3a C3b Anaphylotoxin2,3 Initiates mast cell degranulation4 Promotes neutrophil-mediated acute phase reactions5 driven by pro-inflammatory cytokines6 – particularly IL-6 in gMG7 Has the potential to directly act on NMJ via smo

  73. Slide 73: Classical pathway / aC1s inhibition has the potential to change the CIDP landscape

    Classical pathway / aC1s inhibition has the potential to change the CIDP landscape aC1s inhibitors enroll a broad patient population including SOC-refractory patients ≥1-point aINCAT improvement used as efficacy measure in ongoing studies No requirement for disease worsening in ongoing complement tr

  74. Slide 74: Senior Management and Board of Directors

    SENIOR MANAGEMENT Accomplished team of biotech industry veterans and scientists committed to bringing innovation to market Select Experience Includes: BOARD OF DIRECTORS Alison Lawton Chair of the Board Board Member, ProQR and X4, Prior Chair of Board, Magenta Sujay Kango Board Member, Adanate, Inc.

Dianthus Therapeutics — Investor Presentation (January 2026) on 6ix