Acumen Safe Harbor Statement NOTES REGARDING THIS PRESENTATION This presentation may contain "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995 relating to our busines

Corporate Overview 3Q 2021 Exhibit

Acumen Safe Harbor Statement NOTES

REGARDING THIS PRESENTATION This presentation may contain "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995 relating to our business, operations, and financial conditions, including

but not limited to current beliefs, expectations and assumptions regarding the future of our business, future plans and strategies, our clinical results, our development plans, our intellectual property and other future conditions. Words such as,

but not limited to, "look forward to," "believe," "expect," "anticipate," "estimate," "intend," "plan," "would," "should" and

"could," and similar expressions or words, identify forward-looking statements. These risks and uncertainties are more fully described in our filings with the Securities and Exchange Commission, including in the section entitled

"Risk Factors" in our Quarterly Report on Form 10-Q filed with the SEC on August 16, 2021 and subsequent reports that we file with the Securities and Exchange Commission. Moreover, we operate in a very competitive and rapidly changing

environment. New risks emerge from time to time. It is not possible for our management to predict all risks, nor can we assess the impact of all factors on our business or the extent to which any factor, or combination of factors, may cause actual

results to differ materially from those contained in any forward-looking statements we may make. In light of these risks, uncertainties and assumptions, we cannot guarantee future results, levels of activity, performance, achievements, or events and

circumstances reflected in the forward-looking statements will occur. Forward-looking statements represent our beliefs and assumptions only as of the date of this presentation. Except as required by law, we undertake no duty to update any

forward-looking statements contained in this release as a result of new information, future events, changes in expectations or otherwise. Certain information contained in this presentation relates to or is based on studies, publications, surveys and

other data obtained from third-party sources and the Company's own internal estimates and research. While the Company believes these third-party sources to be reliable as of the date of this presentation, it has not independently verified, and makes

no representation as to the adequacy, fairness, accuracy or completeness of any information obtained from third-party sources. In addition, all of the market data included in this presentation involves a number of assumptions and limitations, and

there can be no guarantee as to the accuracy or reliability of such assumptions. Finally, while we believe our own internal research is reliable, such research has not been verified by any independent source.

Acumen: Advancing a Potential

Best-In-Class Antibody for Early Alzheimer's disease (Early AD) AD Represents an Enormous Market Driven by High Unmet Need and Recent Scientific and Regulatory Momentum Growing Scientific Consensus Supports Amyloid-Beta Oligomers (A Os)

as the Most Neurotoxic Form of A and a Novel Target for Effective AD Treatment ACU193: First, Clinical-Stage monoclonal antibody (mAb) to Selectively Target A Os and has Promising Pre-Clinical Evidence supporting its Differentiation

Experienced Team of Industry Leaders with AD Drug Discovery, Development, and Regulatory Expertise from Eli Lilly & Co. Phase 1 Clinical Trial Initiated in 2Q 2021 with Proof of Mechanism / Biomarker Data by YE 2022 Series B Crossover Round with

High Quality Investor Syndicate July 2021 $184M IPO WITH HIGH QUALITY INVESTOR SYNDICATE

Experienced in AD drug development

ACUMEN LEADERSHIP TEAM DANIEL O'CONNELL President & CEO JANICE HITCHCOCK, PHD VP Regulatory Affairs RUSSELL BARTON Chief Operating Officer JASNA JERECIC, PHD Analytical Methods Leader, Research Scientist ERIC SIEMERS, MD Chief Medical Officer

ROBERT DEAN, MD, PHD Sr. Development Advisor JAMES SENETAR, MS, PHARM.D., PMP Sr. Clinical Operations Manager MATT ZUGA Chief Financial Officer & Chief Business Officer GEORGE VAUGHN, CPA VP, Finance and Accounting Vaughn & Assoc. Over a

decade of experience working towards a shared goal.

Aduhelm Approved under Accelerated

Approval Pathway First disease-modifying drug approved for Alzheimer's Approved under accelerated approval based on reduction in amyloid beta plaques1 ____________________

1https://www.accessdata.fda.gov/drugsatfda_docs/label/2021/761178s000lbl.pdf Aduhelm approval ushers in new era and regulatory environment for AD drug development Acumen will evaluate biomarkers to support future regulatory submissions

The only approved antibody for AD

preferentially targets amyloid plaques with only limited effects on oligomeric forms of A . Acumen's drug candidate ACU193 targets AbOs. Growing Interest in the Anti-A O Hypothesis Growing understanding of disease mechanisms indicate

that A Os are the most toxic A species and have the potential to be an ideal target for effective AD therapy ____________________ Sources: Adopted From: Selkoe, Hardy EMBO Molecular Medicine, 2016. A Os bind to neurons, impair

synaptic function, contribute to impairment of memory and cognition, and induce tau phosphorylation Inflammatory responses microglial and astrocytic activation A oligomers A monomers Amyloid plaque A fibrils

ACU193 Positioning Relative to

Late-stage and Approved Anti-Ab/plaque mAbs * IgG1 monoclonal antibodies that bind amyloid plaque are associated with high rates of ARIA-E solanezumab IgG1, Ph3 stop, A4, DIAN lecanemab/BAN2401 IgG1, Ph3 Aduhelm/aducanumab* IgG1, Approved 7-Jun-21

ACU193 IgG2m4, Ph1a/b bapineuzumab* IgG1, Ph3, stop gantenerumab* IgG1, Ph3 crenezumab IgG4, Ph3 stop, API A oligomers donanemab* IgG1, Ph2 positive ACU193's High Selectivity for A Os Combined with an Expected Lack of ARIA-related

Safety Concerns Is Anticipated to Provide Superior Cognitive Efficacy Compared to Peers

Upcoming Milestones: ACU193 Development

Plan Expected to Demonstrate Proof of Mechanism by YE 2022 ACU193 Phase 1 Proof of Mechanism results are expected to inform dose selection and regulatory strategy for the Phase 2/3 trial 2023 2022 2021 Open IND Initiate Ph1a/b trial YE 2022: Report

Ph1a/b Proof of Mechanism Safety / ARIA PK Target Engagement Biomarkers 1H 2023: FDA Interaction Initiate Ph2/3 trial

AD Drug Development: Amyloid Hypothesis

CONFIDENTIAL & PROPRIETARY

AD is One of the World's

Largest Unmet Medical Needs AD is a progressive, uniformly fatal neurodegenerative disorder and is the most common form of dementia Memory loss is the key symptom of AD In advanced stages of the disease, complications from severe loss of brain

function - such as dehydration, malnutrition or infection - result in death AD is the sixth leading cause of death in the US Treatment options include cholinesterase inhibitors and an NMDA receptor antagonist, aimed to reduce symptomatic

burden, which have modest benefit along with supportive care Aduhelm (aducanumab) was approved through accelerated access pathway based on a surrogate endpoint AD affects >6M people in the United States and >32M people worldwide Patients

suffering in the later stages of AD require nearly full-time care, resulting in a significant societal and economic burden, with direct healthcare costs estimated to be $355 billion annually in 2021 DISEASE OVERVIEW DISEASE BURDEN UNMET

Emerging data indicate that amyloid

oligomers are the most toxic species and should be preferentially targeted for removal A fibrils Alzheimer's Pathophysiology Previous and current anti-amyloid and related drug targets have attempted to intervene BACE inhibitors

Build-up of amyloid-beta (Ab) is believed to lead to neurodegeneration and dementia Anti-amyloid plaque mAb Tau destabilization Symptomatic and neuroprotective treatments Amyloid (A ) Amyloid plaque A monomers A oligomers g

secretase Inhibitors Anti-monomer Ab mAb Anti-Ab oligomer mAb Tau directed treatments

Recent anti-amyloid mAb results

(anti-Ab/plaque) establish biological foothold for treating disease EFFICACY: Reduced cognitive decline ~11% - 47% at ~18 months TARGET ENGAGEMENT: Positive effects on imaging and fluid biomarkers Potential for current generation anti-Ab/plaque mAbs

to serve as first-in-class' drugs providing foothold for treating patients that can be built upon and/or improved ____________________ Abbreviations: ARIA-E - Amyloid Related Imaging Abnormalities - Edema; BACE - Beta Amyloid

Cleavage Enzyme SAFETY: ARIA-E rates ~10% to ~35%, and higher in genetically predisposed APOE4+ for plaque targeting mAbs Anti-Ab/plaque mAbs, as a class, appear to have positive signal in early AD and leave significant room for improvement The

Continuum of Alzheimer's Disease

Measured Outcome** solanezumab

EXPEDITION 3 (Phase 3) aducanumab EMERGE (Phase 3) aducanumab ENGAGE (Phase 3) lecanemab BAN2401 (Phase 2) donanemab (Phase 2) ADAS-cog -11% -27% -12% -47% -39% ADCS-ADL -15% -40% -18% N.A. -23% CDR-SB -15% -23% 2% -26% -23% MMSE -13% -15% 3% N.A.

-21% iADRS -11% N.A. N.A. N.A. -32% Positive Signals and Proof of Concept from Recent Phase 2-3 AD Anti-Amyloid mAb Studies Percent Slowing of Cognitive/Functional Decline* Note: ENGAGE Post-Protocol Version 4 - at least 14 doses of 10 mg/kg,

High Dose cohort achieved 27% improvement on CDR-SB compared to placebo * Percent Slowing = P[1- [(endpoint score-baseline score)active/(endpoint score-baseline score)placebo]]100%(-1) ** ADAS-cog: Alzheimer's Disease Assessment Scale -

Cognitive Subscale ADCS-ADL: Alzheimer's Disease Cooperative Study - Activities of Daily Living CDR-SB: Clinical Dementia Rating - Sum of Boxes MMSE: Mini-Mental State Examination iADRS: Integrated Alzheimer's Disease Rating Scale "We're

looking for a biological foothold against Alzheimer's that we can build on. And so, these effects are small, but I think they are meaningful, and I hope they're the beginning of a process that we can add to."- Stephen Salloway, MD of Brown

University+ ____________________ +Source: Wall Street Journal, Biogen Details Case for Controversial Alzheimer's Drug, published December 5, 2019

TARGETING AB MONOMERS TARGETING

AMYLOID PLAQUES solanezumab EXPEDITION 3 (Phase 3) aducanumab EMERGE (Phase 3) aducanumab ENGAGE (Phase 3) lecanemab BAN2401 (Phase 2) donanemab (Phase 2) PC Treated PC Low High PC Low High PC High PC Treated ARIA-E 0.2% 0.1% 2.2% 26.1% 34.4% 3.0%

25.6% 35.7% 0.8% 9.9% 0.8% 27.5% ApoE carriers 1.9% 29.8% 42.5% 2.4% 28.7% 41.8% 1.2% 14.6% 3.6% 44.0% ApoE non-carriers 2.9% 18.1% 17.9% 4.3% 17.5% 27.7% 0.0% 8.0% Any ARIA E or H 10.3% 32.8% 41.2% 9.8% 30.7% 40.3% N.A. 8.0% 38.9% TARGETING AB

MONOMERS TARGETING AMYLOID PLAQUES solanezumab EXPEDITION 3 (Phase 3) aducanumab EMERGE (Phase 3) aducanumab ENGAGE (Phase 3) lecanemab BAN2401 (Phase 2) donanemab (Phase 2) PC Treated PC Low High PC Low High PC High PC Treated ARIA-E 0.2% 0.1% 2.2%

26.1% 34.4% 3.0% 25.6% 35.7% 0.8% 9.9% 0.8% 27.5% 1.9% 29.8% 42.5% 2.4% 28.7% 41.8% 1.2% 14.6% 3.6% 44.0% 2.9% 18.1% 17.9% 4.3% 17.5% 27.7% 0.0% 8.0% Any ARIA E or H 10.3% 32.8% 41.2% 9.8% 30.7% 40.3% N.A. 8.0% 38.9% Anti-plaque mAbs demonstrate

dose-related ARIAs that will limit use * PC = Placebo, Low = Low Dose; High = High Dose Shows the absence of ARIA after treatment with antibodies targeting A monomers (solanezumab) in comparison to the increasing presence of ARIA after

treatment at increasing dose levels with antibodies targeting amyloid plaques (aducanumab, BAN2401, and donanemab), indicate that ARIA results from the removal of amyloid plaques around blood vessels and likely does not result, from treatment with

antibodies that target other species of A , i.e. A monomers and A Os. Percent of ARIA Events for Anti-A /plaque mAbs* ARIA-E represents a dose limiting adverse effect for mAbs with plaque binding. Antibodies that avoid ARIAs

should be safer and more feasible to administer and possibly at higher doses.

ACU193's High Selectivity for

A Os, Combined with its Expected Lack of ARIA-related Safety Concerns, Is Anticipated to Provide Superior Efficacy Compared to Peers TARGET SELECTIVITY+ SAFETY PROFILE Company Asset Amyloid plaque A fibrils A monomers A

oligomers Lack of ARIA ACU193 untested Aduhelm aducanumab lecanemab BAN2401 gantenerumab donanemab untested

solanezumab* crenezumab* bapineuzumab* ____________________ *Phase 3 discontinued for primary AD indication + There have

been no head-to-head trials between any of the product candidates listed above. Study designs and protocols for each product candidate were different, and results may not be comparable between product candidates.

ACU193: Our differentiated approach

CONFIDENTIAL & PROPRIETARY

DRUG: ACU193 is a humanized,

affinity-matured, mAb with high selectivity for toxic A Os vs. A monomers (>500x) and amyloid plaques. ACU193 is an IgG2m4 subclass mAb which lacks inflammatory effector functions of other IgG subclasses. POPULATION: Early AD - Mild

Cognitive Impairment and Mild Dementia due to AD (amyloid positive by PET) DOSING: IV infusion every 4 weeks DURATION: Chronic therapy for duration of Early AD VALUE PROPOSITION: Selectivity for toxic A Os is expected to provide superior

cognitive efficacy and improved safety and tolerability relative to non-selective anti-A /plaque mAbs Slow decline of memory and cognition in Early AD Decrease A Os induced synaptic and neuronal network toxicity Slow disease progression

and downstream effects on tau, neurodegeneration, and neuro-inflammation Low rate of ARIA expected Effective as stand-alone therapy or potentially in combination with other symptomatic, anti-inflammatory, and/or tau directed therapies Target Product

Profile: ACU193 Best-in-Class, 1st line, anti-A O, Disease-modifying Immunotherapy for Early AD

ACU193: Extensive Data Package

Supporting Development Nanomolar affinity for A Os, >500-fold greater selectivity for A Os over A monomer, with limited or no discernable binding to vascular amyloid or dense core amyloid plaques Binds broad range of endogenous

A Os present in transgenic mice and human AD samples (binds dimers to mid-sized molecular weight A Os) Active IND Phase 1 started 2Q 2021 Brain penetration and biodistribution demonstrated in multiple species Performs like other

peripherally administered CNS mAbs Dose-dependent effects in multiple in vitro neuroprotection assays Positive memory and behavioral effects in multiple in vivo transgenic mouse models for AD IgG2m4 subclass lacks inflammatory effector function

signaling (C1q, Fc R1, Fc RIII) Microhemorrhage studies show no increased risk of microhemeorrhage GLP studies demonstrated acceptable safety margin for clinical dosing plans SELECTIVITY PHARMACOLOGY PK/PD SAFETY REGULATORY ACU193 is a

promising immunotherapy for Early AD expected to provide meaningful cognitive and functional benefits, slow disease progression, and offer an attractive safety profile

AbOs may consist of 2 to >200 Ab

peptides. AbOs composed of 3 (a) and 18 (b) Ab peptides are depicted below. ____________________ Sources: Kelley et al. J Chem Physics 2008. What is an A Oligomer? AbOs are present in brain in a wide range of sizes (a) (b)

Even in the presence of a large

excess of A monomer, binding of ACU193 to A Os is unchanged Highly selective for A oligomers versus A monomers ACU193 is the First mAb Developed to Selectively Target A Os Binding of ACU193 to A Os >500x binding

to A monomer SELECTIVITY ACU193 selective binding to AbOs is preserved even in the presence of a large excess of Ab monomer which is present in brain - limited target distraction Log [Competing Antigen] M ACU193 Selectivity ACU193

Selectivity in presence of 5 M monomeric A

ACU193 has a greater preference for

AbOs than other mAbs Comparison of A species-mAb complex signals across SEC fractions SELECTIVITY ACU193 binds to a wide range of oligomeric species of Ab that are differentiated from those bound by hu266 (solanezumab) or hu3D6 (bapineuzumab)

AD Hippocampus ThioS/amyloid plaque

AD Hippocampus ACU193/AbOs species ____________________ Sources: E. Cline et al. CTAD 2019. ACU193 is highly selective for A Os versus A plaques ACU193 staining in human AD brain slices ACU193 (red) binds non-Thioflavin S positive Ab

(green) SELECTIVITY ACU193 has little or no binding to thioflavin S positive fibrillar A plaque in human AD brain tissue

PHARMACOLOGY SELECTIVITY After