On a mission to develop treatments that restore cognitive function CORPORATE PRESENTATION Safe harbor statement This document contains forward-looking statements within the meaning of Section 27A of the Securities Act of

On a mission to develop treatments that restore cognitive function CORPORATE PRESENTATION

Safe harbor statement This document contains forward-looking statements within the meaning of Section

27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended.Our forward-looking statements are based on current beliefs and expectations of our management team that involve risks, potential

changes in circumstances, assumptions, and uncertainties, including statements about the anticipated timing of release of topline results of our clinical trials; the progression of our discovery programs into clinical development; and the

business and operations of the Company. We may, in some cases use terms such as "predicts," "believes," "potential," "continue," "anticipates," "estimates," "expects," "plans," "intends," "may," "could," "might," "likely," "will," "should" or

other words that convey uncertainty of the future events or outcomes to identify these forward-looking statements. Each forward-looking statement is subject to risks and uncertainties that could cause actual results to differ materially from

those expressed or implied in such statement. Applicable risks and uncertainties include those related to the possibility that any results of operations and financial condition of the Company reported are preliminary and subject to final audit

and the risks listed under the heading "Risk Factors" and elsewhere in our 2020 Form 10-K filed on February 25, 2021, and our subsequent SEC filings. Investors are cautioned not to place undue reliance on these forward-looking statements. These

forward-looking statements (except as otherwise noted) speak only as of the date of this report, and the Company undertakes no obligation to update these forward-looking statements, except as required by law.

On a mission to develop treatments that restore cognitive function Tapping into a fundamental CNS

signaling pathway with CY6463, a first-in-class, CNS-penetrant sGC stimulator Executing biomarker-guided development strategy in well-defined populations with cognitive impairment Tackling the enormous burden and breadth of cognitive

impairment through an innovative portfolio of indications and molecules

Contents NO-sGC-cGMP is a fundamental CNS signaling pathway CY6463 translational pharmacology

clinical study results Advancing next-generation sGC stimulator program Pipeline centered around improving cognitive function Potential for patient impact: 3 studies underway Executing on our priorities

NO-sGC-cGMP is a fundamental CNS signaling pathway

CY6463 amplifies the fundamental NO-sGC-cGMP signaling pathway CY6463First-in-class BBB-permeable,

positive allosteric modulator of sGCAmplifies endogenous NO-sGC-CGMP signaling to address central aspects of disease pathophysiology Preclinical data and extensive academic work validate the crucial role of the NO-sGC-cGMP pathway in brain

physiology Synaptic plasticity Neuro-inflammation Bioenergetics Vascular function PKG, PDE, ion channels Downstream targets (e.g., CREB, BDNF) Important role in learning and memory

CY6463 improves endpoints relevant to cognition Young Control Aged Control Aged CY6463 R6/2 +

CY6463 46 nM R6/2 + CY6463 7 nM R6/2 WT Morphological plasticity In-vivo learning and memory Ex-vivo LTP Young rat/Vehicle Aged rat/Vehicle Aged rat/CY6463 Young rat/Vehicle Aged rat/Vehicle Aged rat/CY6463 *p<0.05 vs. the

CY6463 amplifies a fundamental CNS signaling pathway NO-sGC-cGMP pathway plays a critical role in brain

functionsGC stimulation with CY6463 amplifies NO-sGC-cGMP signalingMorphological, ex vivo and in vivo data demonstrate important role of sGC in synaptic plasticity, learning and memory, and 6463's ability to restore deficits in these

CY6463 Translational Pharmacology Study Results

CY6463 showed rapid and persistent improvements in multiple independent biomarkers associated with

cognitive impairment In a 15-day study in 24 healthy elderly subjects CY6463 demonstrated: Increased alpha and gamma power Improved N200 latency Faster saccadic eye movement (SEM) reaction time Reduced neuroinflammatory

biomarkers Rapid onset (<15 days) Effect increased with ageBiomarkers linked to AD and aging

Phase 1b translational pharmacology study designed to evaluate CNS activity *due to COVID restrictions,

12 subjects completed only period 1 Healthy elderly population ( 65 years) Objectives washout CY6463 QD CY6463 QD Placebo Placebo 15 days 15 days 24 subjects completed period 1 12 subjects completed both periods* Safety and

tolerabilityPharmacokinetics Target engagementCNS activity

CY6463 showed rapid improvement in biomarkers of cognition Increased alpha and gamma power Faster

saccadic eye movement reaction time Improved N200 latency Alpha power: CY6463 vs. placebo Day 15 Improvement Age (years) Untreated CY6463 treated Time (ms) Time

(sec) p=0.0216 Placebo CY6463 p=0.0216 Improvement 0.02 0.00 -0.02 -0.04 Reduced neuroinflammatory biomarkers In a 15-day study in 24 healthy elderly subjects, CY6463 demonstrated:

Pipeline centered around improving cognitive Function

CY6463 data point to potential in cognition Preclinical CNS pharmacology Potential to improve

cognitive function Neuronal function Neuro-inflammation Bioenergetics Vascular function Increased posterior alpha and gamma power Improved N200 latency Faster saccadic eye movement (SEM) andreaction time Reduced

neuroinflammatory biomarkers in CSF Clinical CNS pharmacology* *In a 15-day study in 24 healthy elderly subjects

Cognitive impairment is a debilitating facet of many CNS diseases Neurodegenerative Alzheimer's

Disease Parkinson's Dementia Lewy Body Dementia Neuropsychiatric Major Depressive Disorder Bipolar Disorder Autism Cancer/chemotherapy-induced cognitive impairment Traumatic brain

injury Stroke Event-related Mitochondrial Leigh Syndrome Kearns-Sayre Syndrome ADv ongoing CIAS ongoing MELAS ongoing ~2M ~35M ~13M ~5M Orphan Orphan Orphan ~21M ~150M ~27M ~10M ~21M (US) ~12M ~5M (US) Represents

approximate prevalence of patients with cognitive impairment associated with other CNS diseases, worldwide in millions, except where noted as US prevalence References on file.

Biomarker-guided development strategy in well-defined populations with cognitive impairment ADv |

Alzheimer's Disease with vascular pathology (ADv) CIAS | Cognitive Impairment Associated with SchizophreniaMELAS | Mitochondrial Encephalomyopathy, Lactic Acidosis, and Stroke-like episodes MELAS ADv Neurodegenerative Parallel studies

in distinct populations Efficient, signal-seeking studies inform larger and longer studies Disease-relevant biomarkers accelerate and guide development Improving Cognition Neuropsychiatric CIAS Mitochondrial Disease Significant

additional opportunities Translation of insights across programs increases odds of success

Potential for patient impact: our priority indications

DISCOVERY IND-ENABLING PHASE 1* PHASE 1b/2a PHASE

2 CY6463 MELAS ADv CIAS Multiple under assessment CY3018 Multiple under assessment Advancing parallel, signal-seeking, exploratory studies in priority patient

populations *Two phase 1 studies were completed in healthy young and old (>65 years of age) volunteers confirming targeted CNS exposure and activity

Growing patient population, devastating impact, limited treatments Biomarker-guided development

strategy: ADv Exploratory Phase 2Near-term impact on disease-specific biomarkers and cognition Larger, longer studies symptomatic trialsfocused on cognition Initial approval expected on surrogate, symptomatic or functional endpoints Standard

of carefor patients with ADv Potential for disease modification and expansion into broader AD Today Tomorrow Future Alzheimer'sDisease VascularDementia ADv

ADv study ongoing 20 Exploratory, signal-seeking study to evaluate safety, tolerability,

and pharmacodynamic effects (EEG, MRI, neuroinflammatory biomarkers, cognition) Once-daily CY6463 vs. placebo12 weeks30 participants Confirmed AD pathology (PET, CSF)2+ cardiovascular risk factorsMild-moderate subcortical small-vessel disease

on MRIMini mental state exam score (20-26) Objectives Study design Patient targeting Partially funded by the Alzheimer's Association's Part the Cloud-Gates Partnership Collaborating with Dr. Andrew Budson at Boston University on a study to

examine the relationship between ERP/EEG and cognitive measures in dementias Collaborations

Biomarker-guided development strategy: MELAS Exploratory Phase 2Near-term impact ondisease-specific

biomarkers Larger, longer symptomatic trials focused on cognition and stroke-like-episodes Potential for accelerated approvalwith predictive biomarker Transformative therapy for patients with MELAS Potential for expansion into additional

mitochondrial diseases Today Tomorrow Future MELAS is a serious orphan disease, with significant CNS impact, no approved treatments

MELAS study ongoing; data expected 1H 2022 22 Objectives Exploratory, signal-seeking study to

evaluate safety, tolerability, and pharmacodynamic effects (MRI, biomarkers) Study design 29-day open label Once-daily CY6463Up to 20 adults (targeting 12 completers) Patient targeting Genetically confirmed mitochondrial disease with

neurological features of MELAS Elevated plasma lactate (disease biomarker) Sites and collaborations Study performed at centers of excellence for mitochondrial medicine: CHOP, MGH, Children's National Hospital, Columbia University, Johns

Hopkins University Preclinical collaboration with Dr. Marni Falk at CHOP to elucidate the role of sGC in mitochondrial disease models

Biomarker-guided development strategy: CIAS Exploratory Phase 1bSafety + near-term impact on

disease-relevant biomarkers Larger, longer studies focused on biomarker-identified populations Standard of care adjunctive therapy Improve cognitive impairment and functional outcomes Today Tomorrow Future CIAS is a debilitating

and untreated facet of schizophrenia, with large and growing unmet need

CIAS study ongoing 24 Objectives Exploratory, signal-seeking study to evaluate safety, tolerability,

and pharmacodynamic effects (qEEG, ERP, digital cognitive performance battery) Study design 14-day in clinic, randomized, placebo-controlled, double-blinded Once-daily CY6463Approximately 60 participants across sequential cohorts Patient

targeting Psychiatrically stable adults with schizophreniaOn stable antipsychotic regimen

Next generation sGC stimulator program

Next generation sGC stimulator CY3018: selectively targeting the CNS Greater relative CNS

exposure Greater relative CNS pharmacology Greater CSF:plasma ratio for CY3018 translating into greater relative CNS pharmacologyCY3018 is progressing though IND-enabling developmentOngoing pharmacology studies to validate amenable CNS

indications CY3018 Data displayed as mean+ SEM, Relative pharmacology ratio: 1-hour post-dose with vehicle-subtraction

Executing on our priorities

2021: executing on our priorities 28 * Preliminary, unaudited unrestricted cash, cash equivalents and

restricted cash balance as of March 31, 2021 Clinical andpre-clinical ADv Ph2 study ongoingMELAS Ph2 study data expected H1 2022CIAS Ph1b study ongoingAdvancing CY3018, next-generation development candidate Partnerships Explore CNS

collaborationsPraliciguat out-license complete Capabilities and capital Grow external CNS network and augment coreteam CNS expertiseReduced monthly cash use to ~50% that of 2020Q2 2021 ending cash balance of ~$70M

On a mission to develop treatments that restore cognitive function Tapping into a fundamental CNS

signaling pathway with CY6463, a first-in-class, CNS-penetrant sGC stimulator Executing biomarker-guided development strategy in well-defined populations with cognitive impairment Tackling the enormous burden and breadth of cognitive

impairment through an innovative portfolio of indications and molecules

Appendices Preclinical, Phase 1 and translational pharmacology studies, references

CY6463 demonstrated beneficial effects in preclinical studies across multiple domains associated with

cognitive disease 32 Cerebral Blood FlowIncreased blood flow in areas associated with memory and arousal by fMRI BOLD imaging IMPROVED CellularBioenergeticsIncreased ATP and restored gene expression in cells from patients with

mitochondrial diseases ENHANCED Neuronal FunctionEnhanced memory & spine density in aged animals; increased LTP in neurodegenerative models; affected qEEG spectra IMPROVED Neuro- inflammationDecreased markers of LPS-induced

neuroinflammation (ICAM1, VCAM1, IL6) in vitro REDUCED

CY6463 improved neuronal function Restored hippocampal long-term potentiation to wild-type levels in a

mouse neurodegenerative model Wild type Disease Disease + CY6463 (46 nM) * Normalized fEPSPAmplitude Time (min) 10 30 50 70 1.0 5 2.0 2.5 ImproveNeuronal Function ReduceNeuroinflammation EnhanceCellular

Bioenergetics ImproveCerebral Blood Flow Hippocampal slices from symptomatic Huntington's Disease (R6/2) mice incubated with CY6463 for 25-30 minutes before LTP inductionExtracellular field potentials recordings performed using

Multi-Electrode Array; **p<0.01 vs. Disease By acting directlyon the neurons,CY6463 could restore impaired neurotransmission

CY6463 increased qEEG gamma power No effect seen with PDE9 inhibitor Healthy awake rats were treated

with clinically relevant doses of CY6463 (3 mg/kg) or PDE9 inhibitor (10 mg/kg) Graph displays 1-2h post-dose, mean SEM ImproveNeuronal Function ReduceNeuroinflammation EnhanceCellular Bioenergetics ImproveCerebral Blood Flow CY6463

isdifferentiated from PDE9 inhibitor, which showed no effect on gamma power Gamma Power Vehicle PDE9i CY6463 CY6463 + PDE9i

CY6463 and donepezil act independently to enhance qEEG signal Combination elicited additive increase in

gamma band power in healthy rats ImproveNeuronal Function ReduceNeuroinflammation EnhanceCellular Bioenergetics ImproveCerebral Blood Flow *p<0.05 vs Veh# p<0.05 CY6463 vs CY6463 +DonepezilHealthy rats orally administered CY6463

(10mg/kg), Donepezil (1mg/kg), or a combination. Graph displays 1-2h post-dose, mean SEM CY6463 may offer opportunity to enhance attention and cognitive performance alone and on top of standard of care Gamma

Power Vehicle Donepezil CY6463 CY6463 + Donepezil

CY6463 improved learning and memory in aged rats Increased rate of learning in aged rats treated with

CY6463 in Morris Water Maze Healthy aged male rats were administered CY6463 (10 mg/kg, p.o.) daily during Morris Water Maze training Young rat/Vehicle Aged rat/Vehicle Aged rat/CY6463 Young rat/Vehicle Aged rat/Vehicle Aged

rat/CY6463 *p<0.05 vs. Aged vehicle-treated ImproveNeuronal Function ReduceNeuroinflammation EnhanceCellular Bioenergetics ImproveCerebral Blood Flow

CY6463 improved cognitive function in pharmacologically impaired rats ImproveNeuronal

Function ReduceNeuroinflammation EnhanceCellular Bioenergetics ImproveCerebral Blood Flow Rat Novel Object Recognition *p<0.05 vs. VEH + MK-801 rats CY6463 acts downstream of NMDA receptor to reverse deficit induced by NMDA