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Samus Therapeutics, Inc.

The Epichaperome Inhibitor Company

Forward-Looking Statements

This presentation contains certain forward-looking information about Samus Therapeutics, Inc. that is intended to be covered by the safe harbor for “forward-looking statements” provided by the Private Securities Litigation Reform Act of 1995, as amended. Forward-looking statements are statements that are not historical facts, and in some cases can be identified by terms such as “may,” “will,” “could,” “expects,” “plans,” “anticipates,” “forecasts,” and “believes.” These statements include, but are not limited to, statements regarding the progress, timing and results of preclinical and clinical trials involving the Company’s drug candidates, and the progress of the Company’s research and development programs. All of such statements are subject to certain risks and uncertainties, many of which are difficult to predict and generally beyond the control of the Company, that could cause actual results to differ materially from those expressed in, or implied by, the forward-looking statements. These risks and uncertainties include, but are not limited to whether any of our therapeutic candidates will advance further in the preclinical or clinical trials process and whether and when, if at all, they will receive final approval from the U.S. Food and Drug Administration or equivalent foreign regulatory agencies, whether our products will be successfully marketed if approved; the strength and enforceability of our intellectual property rights; and competition from other pharmaceutical and biotechnology companies. While Samus may elect to update these forward-looking statements at some point in the future, it specifically disclaims any obligation to update or revise any forward-looking-statements contained in this press release whether as a result of new information or future events, except as may be required by law.

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Samus Scientific Platform: Epichaperome Inhibition

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With specific cell stress, chaperomes and client proteins are rewired into the epichaperome.

Inhibitors PU-AD and PU-H71 target Hsp90 in the epichaperome to address the breakdown of regulatory pathways that prevent the aggregation and

accumulation of disease associated aberrant proteins.

Courtesy Gabriela Chiosis

Propagation of Disease

PU-AD and PU-H71 Competitive Inhibitors of ATP BindingDistinct from Historical Hsp90 Inhibitors

HSP90 N-Terminal ATP Binding Pocketwith ATP bound

HSP90 N-TerminalATP Binding Pocketwith PU-H71 bound

ATP PU-H71PU-AD

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Epichaperome Inhibitors PU-AD and PU-H71

• In neurodegenerative disease, PU-AD restores regulatory pathways and initiates degration of client proteins, tau in Alzheimer’s disease.

• While in cancer, PU-H71 initiates degradation of oncogenic proteins, JAK2 in myelofibrosis, and induces apoptosis.

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Cell death in cancer

Neuron survival neurodegenerative diseases

Epichaperome Inhibition Broad Scientific PlatformPrincipal Focus Neurodegenerative Diseases

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• PU-AD Clinical stage

-- Phase 1 SAD/MAD in healthy volunteers (safety and PK) completed

-- Alzheimer’s disease initiating Phase 2a 1H 2020

• PU-AD Preclinical stage

-- Lewy-body/Parkinson's dementia modeling

-- Moderate/severe Traumatic Brain Injury (TBI) modeling

• PU-H71 platform-related clinical stage trial

-- Phase 1b ongoing in myelofibrosis

PU-AD inPreclinical Study in

Alzheimer’s Disease

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PU-AD highly permeable to BBB

• Selective for diseased cells with little/no effect on normal cells (therapeutic doses)

Efficacy in mouse models of tauopathies, AD, Parkinson’s, and in human AD neurons in vitro:

• Significantly improved spatial learning

• Restored long-term memory to parameters in wild type mice

• Restored synaptic plasticity

• Reduced tau pathology

• Increased survival in PS19 mice

PU-AD Alzheimer’s Clinical Development: Stabilize Early Disease

• Phase 1 (oral liquid) SAD/MAD completed in healthy/elderly volunteers for safety and PK

• Phase 2a (daily tablet) to initiate in Alzheimer’s patients 1H 2020

• Phase 2a to address mild AD dementia for target confirmation, changes in biomarkers and early cognition and functionality (activities of daily living)

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Major Neurodegenerative

Diseases Can Be Defined by Four Rogue

Proteins: Tau, Aβ, α-syn, or TDP-43(University of Pennsylvania)

Neurodegenerative Disease Platform:

3 of 4 Rogue Proteins Clients of

Epichaperome;

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•Alzheimer’s Disease: ptau, p35/cdk5, glycogen synthase kinase, MAPK2,Aβ

•ALS: mtau, SOD-1, TDP-43, FUS

•Huntington’s Disease: huntingtin

•Lewy-body and Parkinson’s Dementia*: mtau, α-synuclein, LRRK2

•Pick’s Disease: mtau

•Progressive Nuclear Palsy: mtau

•Frontotemporal Dementia with Parkinsonism linked to chromosome 17: mtau

•TBI, Concussion, CTE*: mtau

* In pre-clinical development

PU-H71 Active, Well-tolerated in IV Phase 1 Extensively Pretreated Patients

• Two myelofibrosis patients in combination stable for 25/36 months with significant symptomatic improvement and improved WBC and Hgb trends

IV Phase 1b in Combination

• One of four patients with extended stable symptoms as in Phase 1; IV PU-H71 and oral ruxolitinib dosing challenging, trial closed to enrollment

PU-H71 now in Oral/Oral Phase 1b trial at 6 sites with CR in transformed AML compassionate care patient further support for myelofibrosis program

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PU-H71 Epichaperome Inhibition in MyelofibrosisCombination Therapy with Ruxolitinib

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Samus Therapeutics – The

Epichaperome Inhibition Company

• PU-AD in Alzheimer’s disease initiating Phase 2a

• Broad application with PU-AD for neurodegenerative/brain diseases

• PU-H71 Orphan Drug Phase 1b in myelofibrosis

• Broad and diverse patent estate

• Experienced leadership and advisory teams

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TM

Samus Therapeutics, Inc.

Epichaperome Inhibitors to TreatNeurodegenerative Disease and Cancer