Keros Therapeutics, Inc. · NASDAQ:KROS

Keros Therapeutics — Investor Presentation (November 2026)

24 slides from Keros Therapeutics's investor presentation, Nov 5, 2026

  1. Slide 1: November 2026 Corporate Presentation

    November 2026 Corporate Presentation

  2. Slide 2: Forward-looking statements

    Corporate Presentation Statements contained in this presentation regarding matters that are not historical facts are “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995, as amended. Words such as "anticipates," "believes," "expects," "intends," “pl

  3. Slide 3: Focused on Transforming the Lives of Patients with Disorders Linked to TGF-β Signaling

    Duchenne Muscular Dystrophy (DMD) N O N C L I N I C A L Corporate Presentation Focused on Transforming the Lives of a Wide Range of Patients with Disorders Linked to Dysfunctional TGF-β Superfamily Signaling We believe our product candidates have the potential to unlock the full therapeutic benefits

  4. Slide 4: Rinvatercept (KER-065)

    Corporate Presentation Rinvatercept (KER-065) 4

  5. Slide 5: Rinvatercept is an investigational modified activin receptor type II ligand trap

    Corporate Presentation 5 Rinvatercept (KER-065) Rinvatercept is an investigational modified activin receptor type II ligand trap Rinvatercept is designed to bind and inhibit TGF-ß ligands, including activin A and myostatin, which are negative regulators of muscle and bone mass and strength, in order

  6. Slide 6: Rinvatercept: Potential to Treat a Broad Range of Neuromuscular Diseases

    Corporate Presentation 6 Rinvatercept: Potential to Treat a Broad Range of Neuromuscular Diseases Created with BioRender Based on observed pharmacology in nonclinical studies and the Phase 1 clinical trial, we believe rinvatercept has potential in multiple, rare neuromuscular diseases with high unme

  7. Slide 7: Rinvatercept: Duchenne Muscular Dystrophy (DMD)

    Corporate Presentation Rinvatercept: Duchenne Muscular Dystrophy (DMD) 7

  8. Slide 8: Duchenne Muscular Dystrophy overview

    1. Tabebordbar, M., et al. (2013). Annu. Rev. Pathol. 8, 441–475. doi: 10.1146/annurev-pathol-011811-132450; 2.Wallace, G. Q., and McNally, E. M. (2009). Annu. Rev. Physiol. 71, 37–57. doi:10.1146/annurev.physiol.010908.1632164.4; 3. Mann, C. J.,et al. (2011). Skelet. Muscle 1:21. doi: 10.1186/2044-

  9. Slide 9: Current Treatment Landscape for DMD

    HDAC Inhibitors • Modulate the deregulated activity of HDACs in dystrophic muscle • DuvyzatTM (givinostat) was approved by the FDA in patients aged 6+ • DuvyzatTM can cause dose-related thrombocytopenia and other signs of myelosuppression, including anemia and neutropenia Corporate Presentation 9 Cu

  10. Slide 10: Robust Nonclinical Data Suggests Potential Benefits of Rinvatercept Through Activin A Inhibition

    Corporate Presentation 10 Robust Nonclinical Data Suggests Potential Benefits of Rinvatercept Through Activin A Inhibition D2.MDX = mouse model of DMD Created with BioRender ✓ Offer greater muscle and fat benefits: Potential to increase muscle mass and decrease fat mass beyond myostatin alone, based

  11. Slide 11: Rinvatercept Was Generally Well Tolerated in Phase 1 Healthy Volunteer Trial

    Corporate Presentation 11 Treatment with Rinvatercept Was Generally Well Tolerated in Phase 1 Healthy Volunteer Trial ▪ Most TEAEs were mild (Grade 1) to moderate (Grade 2) ▸ One unrelated Grade 4 TEAE (transient CK elevation)* was observed ▪ No dose-limiting toxicities or serious adverse events wer

  12. Slide 12: Phase 1 Healthy Volunteer Data Support Potential to Address Multiple Aspects of DMD

    Corporate Presentation 12 Phase 1 Healthy Volunteer Data Support Potential for Rinvatercept to Address Multiple Aspects of DMD Muscle Bone Fat In DMD, the replacement of muscle fibers with fatty and fibrotic tissue leads to progressive loss of muscle strength and function, leading to immobility and

  13. Slide 13: Rinvatercept: Phase 2 Clinical Trial Design

    11 Endpoints • Primary • Safety and Tolerability • Key Secondary • Pharmacokinetics • Anti-drug antibodies • Body composition • Comprehensive functional improvements (skeletal muscle, motor, cardiac and pulmonary) • Exploratory • Serum Biomarkers Rinvatercept: Phase 2 Clinical Trial Design PK = phar

  14. Slide 14: Rinvatercept: Amyotrophic Lateral Sclerosis (ALS)

    Corporate Presentation Rinvatercept: Amyotrophic Lateral Sclerosis (ALS) 14

  15. Slide 15: Rinvatercept and ALS: A Novel Approach

    1. Brown, R.H. et al, NEJM 2017, 162-172; 2. Mehta P. et al, Amyotrophic Lateral Scler. Frontotemporal Degener. 2025, 290-295 ▪ ALS is a progressive, neurodegenerative disease that destroys motor neurons, leading to muscle weakness, loss of function and eventually paralysis1 ▪ In the U.S. alone, ALS

  16. Slide 16: Potential Benefits of Rinvatercept Treatment for Individuals with ALS

    Potential Benefits of Rinvatercept Treatment for Individuals with ALS Corporate Presentation 16 We plan to engage regulators on the design of this Phase 2 clinical trial evaluating rinvatercept in patients with ALS in the second half of 2026 1. Duranti, E. The Role of Skeletal Muscle in Amyotrophic

  17. Slide 17: Third-Party Myostatin Inhibitor Data Demonstrated Muscle Preservation Can Provide Functional Benefit

    Corporate Presentation 17 Third-Party Myostatin Inhibitor Data Demonstrated That Muscle Preservation Can Provide Functional Benefit 1. Crawford, T. et al; Lancet Neurology 2025, v.24, 9, 727-739 HFMSE = Hammersmith Functional Motor Scale Expanded Motor neuron loss is a hallmark of both spinal muscul

  18. Slide 18: RKER-065 Preserved Muscle Strength and Neuromuscular Transmission in ALS Mouse Model

    RKER-065 Treatment Preserved Muscle Strength and Neuromuscular Transmission in a Mouse Model of ALS Six-week-old male SOD1-G93A (SOD1) mice (mouse model of ALS) were intraperitoneally injected with vehicle or RKER-065 (10 mg/kg, BIW) for 8 weeks. Vehicle-treated wild-type mice served as a control gr

  19. Slide 19: RKER-065 Protected the Neuromuscular Junction in a Mouse Model of ALS

    In healthy neuromuscular junctions (NMJs), there is a normal complement of neurofilaments at the axon terminal RKER-065 Treatment Protected the Neuromuscular Junction in a Mouse Model of ALS SOD1-G93 Mouse Model of ALS Corporate Presentation 19 NF-H: (neurofilament protein-heavy) marker of axon inte

  20. Slide 20: Elritercept (KER-050)

    Corporate Presentation 20 Elritercept (KER-050)

  21. Slide 21: Global License Agreement with Takeda Pharmaceuticals

    Corporate Presentation Global License Agreement with Takeda Pharmaceuticals Keros entered into an exclusive license agreement with Takeda to develop, manufacture and commercialize elritercept globally, other than mainland China, Hong Kong, and Macau 21 Keros received an upfront payment of $200 milli

  22. Slide 22: Proprietary Discovery Approach

    Corporate Presentation Proprietary Discovery Approach 22

  23. Slide 23: Proprietary Discovery Approach

    Proprietary Discovery Approach Keros has a broad approach to target the TGF-β superfamily to develop product candidates with the potential to treat a broad range of indications, including neuromuscular and neurodegenerative disorders, rare bone and fibrosis diseases and obesity/frailty Rinvatercept,

  24. Slide 24: KER-206 Has the Potential to Increase Bone Mass and Improve Skeletal Integrity

    Corporate Presentation KER-206 is a nonclinical asset that was nominated out of our proprietary library of ActRII ligand traps for further investigation: • Novel ligand trap comprised of a modified ligand-binding domain derived from ActRIIB that is fused to the portion of the human antibody known as

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