Acumen Pharmaceuticals (NASDAQ: ABOS) secures $35.75M to advance EBD Alzheimer’s program

Rhea-AI Filing Summary

Acumen Pharmaceuticals is raising about $35.75 million through a private placement of 10,833,331 common shares at $3.30 per share with institutional investors. The deal is expected to close on March 16, 2026, subject to customary conditions. The company plans to use the proceeds primarily to advance its Enhanced Brain Delivery (EBD™) program, including preclinical work to select a lead clinical candidate, and for working capital and general corporate purposes. Acumen also granted investors registration rights to resell the new shares after the company files and clears a resale registration statement.

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Biotech equity analyst

Acumen secures $35.75M to advance its EBD Alzheimer’s pipeline while adding equity dilution.

Acumen Pharmaceuticals has structured a private placement of $35.75 million by issuing 10,833,331 common shares at $3.30 per share to institutional and accredited investors. The financing is aligned with the company’s focus on amyloid beta oligomer–targeting therapies for Alzheimer’s disease.

The company states that proceeds will primarily support its Enhanced Brain Delivery (EBD™) program, including preclinical work toward nominating a lead clinical candidate, alongside working capital and other corporate needs. This adds to a previously disclosed cash and securities balance of $136M as of September 30, 2025, which management expects to fund operations into early 2027.

The Registration Rights Agreement obligates Acumen to file a resale registration statement shortly after its Form 10‑K for the year ended December 31, 2025, and to keep it effective until investors can sell under Rule 144 or have sold the registered shares. Actual market impact will depend on closing of the placement and future resale activity.

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UNITED STATES

SECURITIES AND EXCHANGE COMMISSION

WASHINGTON, D.C. 20549

FORM 8-K

CURRENT REPORT

Pursuant to Section 13 or 15(d)

of the Securities Exchange Act of 1934

Date of report (Date of earliest event reported): March 13, 2026

Acumen Pharmaceuticals, Inc.

(Exact name of Registrant as Specified in Its Charter)

Delaware			001-40551			36-4108129
(State or Other Jurisdiction of Incorporation)			(Commission File Number)			(IRS Employer Identification No.)

1210-1220 Washington Street, Suite 210 Newton, Massachusetts			02465
(Address of Principal Executive Offices)			(Zip Code)

Registrant’s Telephone Number, Including Area Code: (617) 344-4190

(Former Name or Former Address, if Changed Since Last Report)

Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions (see General Instructions A.2. below):

o			Written communications pursuant to Rule 425 under the Securities Act (17 CFR 230.425)
o			Soliciting material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12)
o			Pre-commencement communications pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR 240.14d-2(b))
o			Pre-commencement communications pursuant to Rule 13e-4(c) under the Exchange Act (17 CFR 240.13e-4(c))

Securities registered pursuant to Section 12(b) of the Act:

Title of each class

Trading Symbol(s)

Name of each exchange on which registered

Common Stock, $0.0001 par value

ABOS

The Nasdaq Global Select Market

Indicate by check mark whether the registrant is an emerging growth company as defined in Rule 405 of the Securities Act of 1933 (§230.405 of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (§240.12b-2 of this chapter).

Emerging growth company  x

If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act.  o

Item 1.01 Entry into a Material Definitive Agreement.

Securities Purchase Agreement

On March 13, 2026, Acumen Pharmaceuticals, Inc. (the “Company”) entered into a Securities Purchase Agreement (the “Purchase Agreement”) with certain institutional accredited investors named therein (each, an “Investor” and collectively, the “Investors”), pursuant to which the Company agreed to sell to the Investors, in a private placement (the “Private Placement”), 10,833,331 shares (the “Shares”) of the Company’s common stock, par value $0.0001 per share (the “Common Stock”), at an offering price of $3.30 per Share. The gross proceeds of the Private Placement are expected to be approximately $35.75 million, before deducting applicable fees and other expenses.

The Private Placement is expected to close on March 16, 2026, subject to the satisfaction of customary closing conditions. The Company intends to use the net proceeds from the Private Placement to primarily support its Enhanced Brain Delivery (EBD) program, including ongoing preclinical development work to support the nomination of a lead clinical candidate molecule, and for working capital and other general corporate purposes.

The Purchase Agreement contains customary representations, warranties and agreements by the Company, customary conditions to closing, indemnification obligations of the Company, other obligations of the parties and termination provisions. Pursuant to the Purchase Agreement, the Company has agreed to certain restrictions on the issuance and sale of shares of the Company’s securities for a period beginning on the date of the Purchase Agreement until the earlier of (i) the sixty days after the closing date of the Private Placement and (ii) the business day immediately following the date the resale registration statement filed pursuant to the Registration Rights Agreement (as defined below) becomes effective, subject to certain exceptions.

The Shares to be issued pursuant to the Purchase Agreement have not been registered under the Securities Act of 1933, as amended (the “Securities Act”), or any state securities laws and will be issued pursuant to the exemption from registration provided for under Section 4(a)(2) of the Securities Act. The Company relied on this exemption from registration based in part on representations made by the Investors. The Shares may not be offered or sold in the United States absent registration or an applicable exemption from registration requirements. Neither this Current Report on Form 8-K, nor any exhibit attached hereto, is an offer to sell or the solicitation of an offer to buy the Shares described herein.

Registration Rights Agreement

In connection with the Private Placement, the Company and the Investors entered into a Registration Rights Agreement, dated March 13, 2026 (the “Registration Rights Agreement”), providing for the registration for resale of the Shares pursuant to a registration statement (the “Registration Statement”) to be filed with the Securities and Exchange Commission (the “SEC”) no later than two business days after the date on which the Company files with the SEC its Annual Report on Form 10-K for the fiscal year ended December 31, 2025. The Company has agreed to use reasonable best efforts to cause the Registration Statement to be declared effective as soon as practicable, but in any event no later than the earlier of (i) the 75th calendar day following the initial filing of the Registration Statement if the SEC notifies the Company it will “review” the Registration Statement and (ii) the fifth business day after the date the Company is notified (orally or in writing, whichever is earlier) by the SEC that the Registration Statement will not be “reviewed” or will not be subject to further review, and to keep the Registration Statement continuously effective from the date on which the SEC declares the Registration Statement to be effective until (i) the date on which the Investors shall have resold all the Registrable Securities (as such term is defined in the Registration Rights Agreement) covered thereby, and (ii) the date on which the Registrable Securities may be resold by the Investors without registration and without regard to any volume or manner-of-sale limitations by reason of Rule 144 as promulgated by the SEC under the Securities Act (“Rule 144”), without the requirement for the Company to be in compliance with the current public information requirement under Rule 144 under the Securities Act or any other rule of similar effect.

The Company has granted the Investors customary indemnification rights in connection with the Registration Rights Agreement. The Investors have also granted the Company customary indemnification rights in connection with the Registration Rights Agreement.

The foregoing descriptions of the Purchase Agreement and the Registration Rights Agreement are not complete and are qualified in their entirety by reference to the full text of the Purchase Agreement and Registration Rights Agreement, which are filed as Exhibits 10.1 and 10.2, respectively, to this Current Report on Form 8-K and are incorporated by reference herein.

Item 3.02 Unregistered Sales of Equity Securities.

The information contained in Item 1.01 of this Current Report on Form 8-K is incorporated by reference into this Item 3.02.

Neither this Current Report on Form 8-K nor any exhibit attached hereto is an offer to sell or the solicitation of an offer to buy any securities of the Company.

Item 7.01     Regulation FD Disclosure.

On March 16, 2026, the Company issued a press release announcing the Private Placement and certain preclinical data, including in vitro, in vivo and non-human primate study results, that support development candidates in the Company’s transferrin-receptor targeting EBD program. The press release is attached as Exhibit 99.1 to this Current Report on Form 8-K.

On March 16, 2026, the Company posted an updated corporate presentation to its website at https://investors.acumenpharm.com/news-events/presentations, which the Company may use from time to time in communications or conferences. The corporate presentation was updated to include a summary of the preclinical non-human primate data from the Company’s EBD program. A copy of the presentation is attached as Exhibit 99.2 to this Current Report on Form 8-K.

The information in this Item 7.01, including Exhibit 99.1 and Exhibit 99.2 attached hereto, shall not be deemed “filed” for purposes of Section 18 of the Securities Exchange Act of 1934, as amended, or otherwise subject to the liabilities of that section, nor shall it be deemed incorporated by reference in any filing under the Securities Act of 1933, as amended, except as expressly set forth by specific reference in such filing. The Company’s submission of this Report shall not be deemed an admission as to the materiality of any information required to be disclosed solely to satisfy the requirements of Regulation FD.

Note Regarding Forward-Looking Statements

This Current Report on Form 8-K includes forward-looking statements. These forward-looking statements generally can be identified by the use of words such as “anticipate,” “expect,” “plan,” “could,” “may,” “will,” “believe,” “estimate,” “forecast,” “goal,” “project,” and other words of similar meaning. These forward-looking statements address various matters, including the expected closing date of the Private Placement and the expected use of proceeds from the Private Placement. Each forward-looking statement contained in this Current Report on Form 8-K is subject to risks and uncertainties that could cause actual results to differ materially from those expressed or implied by such statement. Applicable risks and uncertainties include, among others, the risk that the conditions to closing of the Private Placement are not satisfied; that the development and commercialization of our product candidates may take longer or cost more than planned, including as a result of conducting additional studies or our decisions regarding execution of such commercialization; that raising additional capital may cause dilution to our stockholders; that our product candidates may not receive regulatory approval, become commercially successful products, or result in new treatment options being offered to patients; and the risks identified under the heading “Risk Factors” in our Annual Report on Form 10-K for the fiscal year ended December 31, 2024, and filed with the SEC, as well as the other information we file with the SEC. We caution investors not to place considerable reliance on the forward-looking statements contained in this presentation. You are encouraged to read our filings with the SEC for a discussion of these and other risks and uncertainties. The forward-looking statements in this Current Report on Form 8-K speak only as of the date hereof, and we undertake no obligation to update or revise any of these statements. Our business is subject to substantial risks and uncertainties, including those referenced above. Investors, potential investors, and others should give careful consideration to these risks and uncertainties.

Item 9.01    Financial Statements and Exhibits.

Exhibit No.						Description
10.1*						Form of Securities Purchase Agreement, dated March 13, 2026, by and among Acumen Pharmaceuticals, Inc. and the investors party thereto
10.2						Form of Registration Rights Agreement, dated March 13, 2026, by and among Acumen Pharmaceuticals, Inc. and the investors party thereto
99.1						Press release issued by Acumen Pharmaceuticals, Inc. on March 16, 2026, related to the Private Placement
99.2						Corporate Presentation, dated March 16, 2026
104						Cover Page Interactive Data File (embedded within the Inline XBRL document)

* Certain schedules, exhibits and similar attachments have been omitted pursuant to Item 601(a)(5) of Regulation S-K. The Company will provide a copy of such omitted materials to the SEC or its staff upon request.

SIGNATURES

Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.

			Acumen Pharmaceuticals, Inc.
Dated: March 16, 2026			By:			/s/ Derek Meisner
						Derek Meisner Chief Legal Officer

Exhibit 99.1

Acumen Pharmaceuticals Announces $35.75 Million Private Placement to Advance Potential Best-in-Class Molecules from Amyloid Beta Oligomer-Selective Enhanced Brain Delivery Portfolio

•Financing demonstrates conviction in oligomer-selective approach and follows strong preclinical data, including in vitro, in vivo and non-human primate study results, that support development candidates in Acumen’s transferrin-receptor targeting Enhanced Brain Delivery (EBDTM) program

•Candidates exceeded key preclinical criteria, demonstrating elevated brain exposure in non-human primates up to 40-fold over native antibodies, low risk of anemia, and robust stability profiles to enable subcutaneous administration

•Lead clinical candidate IND targeted for mid-2027

NEWTON, Mass., Mar. 16, 2026 – Acumen Pharmaceuticals, Inc. (NASDAQ: ABOS) (“Acumen” or the “Company”), a clinical-stage biopharmaceutical company developing novel therapeutics that target toxic soluble amyloid b oligomers (AβOs) for the treatment of Alzheimer’s disease (AD), today announced that it has entered into a securities purchase agreement with certain institutional and accredited investors for a private placement of approximately $35.75 million of shares of its common stock at a price of $3.30 per share. Acumen expects to receive gross proceeds from the offering of approximately $35.75 million, before deducting offering expenses.

“This financing from committed institutional investors strongly validates our portfolio and our Enhanced Brain Delivery strategy,” said Daniel O’Connell, Chief Executive Officer of Acumen. “The transaction also underscores confidence in the potential value we are building with amyloid b oligomer-targeted antibodies for Alzheimer’s patients, caregivers and stakeholders in alignment with Acumen’s vision.”

The private placement was led by existing investor RA Capital Management, with participation from other investors, including ADAR1 Capital Management, Sands Capital, and a large investment management firm.

The private placement is expected to close on or about March 16, 2026, subject to the satisfaction of customary closing conditions.

Proceeds from the financing are expected to primarily support Acumen’s Enhanced Brain Delivery (EBD) program, including ongoing preclinical development work to support the nomination of a lead clinical candidate molecule, and for working capital and other general corporate purposes. Submission of an IND with respect to a lead clinical candidate is targeted for mid-2027.

The securities to be sold in the private placement have not been registered under the Securities Act of 1933, as amended (the “Securities Act”), or any state or other applicable jurisdictions’ securities laws, and may not be offered or sold in the United States absent registration or an applicable exemption from the registration requirements of the Securities Act and applicable state or other jurisdictions’ securities laws. Acumen has agreed to file a registration statement with the United States Securities and Exchange Commission (the “SEC”) registering the resale of the shares of common stock issued in the private placement, no later than two business days after the filing of its annual report on Form 10-K for the fiscal year ended December 31, 2025.

This press release shall not constitute an offer to sell or the solicitation of an offer to buy these securities, nor shall there be any offer, solicitation or sale of these securities in any jurisdiction in which such offer, solicitation or sale would be unlawful. Any offering of the securities under the resale registration statement will only be made by means of a prospectus.

EBD Non-Human Primate (NHP) Study Results

On March 16, 2026, Acumen also announced certain preclinical data, including in vitro, in vivo and NHP study results, that support development candidates in Acumen’s EBD program, conducted utilizing JCR Pharmaceuticals’ (“JCR”) blood-brain barrier penetrating technology, J-Brain Cargo®. The development candidate results are consistent and predictive across in vitro and in vivo studies, including murine and NHP data. Findings include:

Enhanced Brain Penetration

o    Development candidates achieved 14-40x higher brain levels in NHPs compared to native antibodies at 24 hours

Low Anemia Risk

o    Hematology data in NHPs indicate low potential for anemia with no adverse effects observed

Subcutaneous Dosing Capability

o    Favorable stability profile and enhanced brain delivery support subcutaneous administration with low-volume devices

Acumen’s EBDTM program is part of an ongoing collaboration between Acumen and JCR announced in July 2025. J-Brain Cargo® technology is JCR’s proprietary drug delivery system that efficiently delivers drugs to target tissues, including the central nervous system, through receptor-mediated transcytosis. It is applicable to various modalities including antibodies, enzymes, oligonucleotides, lipid nanoparticles, gene and cell therapy, peptides and decoy receptors.

“We are very pleased with the preclinical EBD candidate profiles generated to date and impressed with the level of expertise contributed by our partner to ensure we exceeded our target profile for the program,” said Jim Doherty, President and Chief Development Officer of Acumen. “Candidates have shown robust in vivo brain penetration in multiple species, hematology endpoints in non-human primates suggestive of a low potential for anemia risk, and stability results supportive of subcutaneous dosing. Ours is the only EBD program in the anti-amyloid space that pairs an Aβ oligomer-targeting antibody with a validated TfR-targeting antibody technology, underscoring an exciting opportunity to develop a potential best-in-class treatment for people living with Alzheimer’s Disease.”

About Acumen Pharmaceuticals, Inc.

Acumen Pharmaceuticals is a clinical-stage biopharmaceutical company developing a novel therapeutic that targets toxic soluble amyloid beta oligomers (AβOs) for the treatment of Alzheimer’s disease (AD). Acumen’s scientific founders pioneered research on AβOs, which a growing body of evidence indicates are early and persistent triggers of Alzheimer’s disease pathology. Acumen is currently focused on advancing its lead investigational product candidate, sabirnetug (ACU193), a humanized monoclonal antibody that selectively targets toxic soluble AβOs, in its ongoing Phase 2 clinical trial ALTITUDE-AD (NCT06335173) in early symptomatic Alzheimer’s disease patients, following positive results in its Phase 1 trial INTERCEPT-AD. Acumen is also investigating a subcutaneous formulation of sabirnetug using Halozyme’s proprietary ENHANZE® drug delivery technology. Acumen is also collaborating with JCR Pharmaceuticals to develop an Enhanced Brain Delivery (EBD™) therapy for Alzheimer’s disease utilizing a transferrin-receptor-targeting blood-brain barrier-penetrating technology. The company is headquartered in Newton, Mass.

About the J-Brain Cargo® Platform Technology

 
JCR Pharmaceuticals has developed a proprietary blood-brain barrier (BBB)-penetrating technology, J-Brain Cargo®, to bring biotherapeutics into the central nervous system (CNS). The first drug developed based on this technology is IZCARGOTM (INN: pabinafusp alfa) and is approved in Japan for the treatment of a lysosomal storage disorder. 

About JCR Pharmaceuticals Co., Ltd.

JCR Pharmaceuticals Co., Ltd. is a global specialty pharmaceutical company that develops treatments that go beyond rare diseases to solve the world’s most complex healthcare challenges. JCR continues to build upon our 50-year legacy in Japan while expanding our global footprint into the US, Europe, and Latin America. JCR’s innovative therapies address conditions like growth disorder, MPS II, Fabry disease, acute graft-versus-host disease, and renal anemia. JCR is also developing treatments for rare diseases like MPS I, MPS II, MPS IIIA and B, and more.

Forward-Looking Statements

This press release contains forward-looking statements within the meaning of The Private Securities Litigation Reform Act of 1995.  Any statement describing Acumen’s goals, expectations, financial or other projections, intentions or beliefs is a forward-looking statement and should be considered an at-risk statement. Words such as “believes,” “expects,” “anticipates,” “could,” “should,” “would,” “seeks,” “aims,” “plans,” “potential,” “will,” “milestone” and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. Forward-looking statements include statements concerning the expected gross proceeds, use of proceeds and anticipated timing for closing of Acumen’s private placement, as well as Acumen’s business, the results and significance of Acumen's preclinical data that support development candidates in the Company’s EBD program, and Acumen’s plans to develop a candidate to treat Alzheimer's Disease utilizing EBD technology, including its expectations with respect to timing for the submission of an IND, as well as its potential for developing a best-in-class therapeutic candidate for people living with Alzheimer’s Disease. These statements are based upon the current beliefs and expectations of Acumen management, and are subject to certain factors, risks and uncertainties, particularly those inherent in the process of discovering, developing and commercializing safe and effective human therapeutics. Such risks may be amplified by the impacts of geopolitical events and macroeconomic conditions, such as rising inflation and interest rates, supply disruptions and uncertainty of credit and financial markets. These and other risks concerning Acumen’s programs are described in additional detail in Acumen’s filings with the Securities and Exchange Commission (“SEC”), including in Acumen’s most recent Annual Report on Form 10-K, and in subsequent filings with the SEC. Copies of these and other documents are available from Acumen.  Additional information will be made available in other filings that Acumen makes from time to time with the SEC. These forward-looking statements speak only as of the date hereof, and Acumen expressly disclaims any obligation to update or revise any forward-looking statement, except as otherwise required by law, whether, as a result of new information, future events or otherwise. 

CONTACTS:

Investors: 

Alex Braun 

abraun@acumenpharm.com 

Media:
ICR Healthcare
AcumenPR@icrhealthcare.com

Corporate Presentation March 2026 1

Forward-Looking Statements 2 This presentation contains forward-looking statements within the meaning of The Private Securities Litigation Reform Act of 1995. Any statement describing Acumen’s goals, expectations, financial or other projections, intentions or beliefs is a forward-looking statement and should be considered an at-risk statement. Words such as “believes,” “expects,” “anticipates,” “could,” “would,” “seeks,” “aims,” “plans,” “potential,” “will” and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. Forward-looking statements include statements concerning Acumen’s business, and Acumen’s ability to achieve its strategic and financial goals, including its projected use of cash, cash equivalents and marketable securities and the expected sufficiency of its cash resources into early 2027, the therapeutic potential of Acumen’s product candidate, sabirnetug (ACU193), including against other antibodies, the timing of anticipated topline results of ALTITUDE-AD, the potential for additional development to support a subcutaneous dosing option of sabirnetug, and the potential to develop a candidate to treat Alzheimer's Disease utilizing EBD technology. These statements are based upon the current beliefs and expectations of Acumen management, and are subject to certain factors, risks and uncertainties, particularly those inherent in the process of discovering, developing and commercializing safe and effective human therapeutics. Such risks may be amplified by the impacts of the COVID-19 pandemic. These and other risks concerning Acumen’s programs are described in additional detail in Acumen’s filings with the Securities and Exchange Commission (“SEC”), including in Acumen’s most recent Annual Report Form 10-K and future filings and reports by Acumen. Copies of these and other documents are available from Acumen. Additional information will be made available in other filings that Acumen makes from time to time with the SEC. These forward- looking statements speak only as of the date hereof, and Acumen expressly disclaims any obligation to update or revise any forward- looking statement, except as otherwise required by law, whether, as a result of new information, future events or otherwise. In this presentation, references to cash also include cash equivalents.

3 Large and growing market in need of additional treatment options Sabirnetug (ACU193): monoclonal antibody (mAb) highly selective for toxic AβOs with positive Phase 1 clinical trial results in AD patients; Phase 2 (IV) topline results expected late 2026 Enhanced Brain Delivery (EBDTM) program to develop oligomer-targeted antibodies with BBB-penetrating technology; EBD pre-clinical candidate (PCC) data announced early 2026 & IND targeted for mid-2027 Experienced leadership team with extensive AD drug development experience Strong balance sheet supporting clinical development plans for sabirnetug ($136M at 9/30/25) BBB: blood-brain-barrier Advancing Next Generation Treatments for Early Alzheimer’s Disease (AD) Targeting Toxic Amyloid Beta Oligomers (AβOs)

Early AD Patient Population Represents Significant and Growing Market STAGES AND CHARACTERISTICS OF AD PROGRESSION Severe DementiaModerate DementiaMild DementiaMild Cognitive ImpairmentPreclinical AD ~5 Million* ~2 Million* Early Alzheimer’s Disease in the U.S. Cognitive Decline Behavioral and Psychological Complications Functional Decline Growing Market Higher prevalence due to aging population More diagnosed cases driven by improved ability to diagnose in earlier stages of AD via increased understanding of blood-based biomarkers More treated cases due to availability of treatment options and favorable shifts around adoption *Alzheimer's Association 4

5 *ARIA-E: Amyloid-related imaging abnormalities - edema AD Treatment Landscape Continues to Evolve Approved Therapies Establish Momentum and Next-generation Approaches Expand Impact Future of AD Landscape Broadens Growth Prospects • New blood-based biomarkers and imaging tools will improve diagnostic and monitoring capabilities • Expansion into preclinical AD will significantly increase the addressable population • Combinations with other targets, such as tau, hold promise Current AD Treatments Offer Hope for People Living with AD • First approved anti-amyloid therapies steadily growing • Education and infrastructure buildout allowing for greater access to treatments by the addressable patient population • Increase efficacy • Reduce ARIA-E* risk • Provide more convenient delivery options • Target amyloid that occurs earlier in disease course Opportunities for New Anti-amyloid Therapies to Strengthen Risk-Benefit Tradeoff

6 Phase 1 Phase 2 Phase 3Preclinical Intravenous (IV) Subcutaneous (SC) Fully enrolled, Phase 2 topline results expected late 2026 Phase 1 topline results announced March 2025 support further development TfR-Brain transporter + anti-AβO mAb (SC) Option to develop up to two EBD development candidates for the treatment of AD; IND targeted for mid-2027 Sabirnetug (ACU193) Enhanced brain delivery (EBDTM) 2026 a Pivotal Year for Acumen’s Pipeline Sabirnetug Global Phase 2 Study Results & Next Generation EBDTM Candidate Selection

Acumen Leadership Team Experienced in AD/Neuro Drug Development Acumen team has decades of experience in Alzheimer’s drug discovery and development AMY SCHACTERLE, PHD Chief Regulatory Officer, Head of Quality PAUL SHUGHRUE, PHD VP, Research & Strategy JASNA JERECIC, PHD Disease Area Strategy Lead ERIC SIEMERS, MD Chief Medical Officer MATT ZUGA Chief Financial Officer & Chief Business Officer RUSSELL BARTON Chief Operating Officer DANIEL O'CONNELL Chief Executive Officer SIEW TIN GAN Head of Clinical Operations 7 JULIE BOCKENSTETTE Chief People Officer JAMES DOHERTY, PHD President & Chief Development Officer LIEAN SCHENK SVP, Head of CMC LAURA ROSEN, MD, PHD SVP, Clinical Development DEREK MEISNER, JD Chief Legal Officer

Milestones Achieved and Upcoming ~$136M Cash, cash equivalents and marketable securities as of Sept. 30, 2025 8 MILESTONES TIMING STATUS Initiation of ALTITUDE-AD Phase 2 trial 2Q2024 ✓ Completion of enrollment of ALTITUDE-AD 1Q2025 ✓ Phase 1 subcutaneous topline results 1Q2025 ✓ EBDTM non-clinical data package Early 2026 ✓ ALTITUDE-AD topline results Late 2026 Acumen expects its cash runway to extend into early 2027

Amyloid Beta Oligomers in AD Sabirnetug (ACU193): monoclonal antibody (mAb) highly selective for toxic AβOs

Soluble AβOs Contribute to Pathophysiological Processes Associated with Alzheimer’s Disease • Toxic consequences of soluble Aβ oligomer production include synapse dysfunction and loss, tau hyperphosphorylation, immune cell activation and functional impairment • Reduced neuronal toxicity and intervention at the synaptic level may prevent irreversible neuronal cell death Aberrant Tau Phosphorylation Selective Neuron Death Oxidative & ER Stress Insulin Resistance ChAT Loss Synaptic Deterioration Plasticity Dysfunction Receptor Redistribution Impact on Astrocytes/Microglia Disrupted Ca2+ homeostasis Inhibition of Axonal Transport 10 Adapted from Blomeke et al. 2024 Model of Aβ oligomer levels • Soluble Aβ forms appear early in the course of disease pathophysiology • Production of toxic soluble Aβ persists after plaque removal

Sabirnetug: Potential Next Generation Immunotherapy for Early AD 11 • Humanized, affinity matured mAb developed to target toxic Aβ oligomers • IgG2 subclass mAb with reduced effector function Designed for Improved Efficacy & Safety Encouraging Regulatory Interactions • FDA Fast Track designation for the treatment of early AD • Phase 2 implemented as a registration- quality study Positive Ph1 in AD Patients & Encouraging Ph2 Enrollment • Successful Phase 1 exclusively in early AD patients ✓ Safety, target engagement, biomarker effects • Phase 2 (n=542) enrollment complete in March 2025; topline results expected in late 2026 Monomers Oligomers Protofibrils Fibrils Plaques Soluble Amyloid Insoluble Amyloid sabirnetug IgG2 Neurotoxic

Sabirnetug

Q2W: Dosing every two weeks; Q4W: Dosing every four weeks. PART A: SINGLE-ASCENDING DOSE n = 8 per cohort (32 total) 6:2 per cohort PART B: MULTIPLE-ASCENDING DOSE n = 10 per cohort (30 total) 3 administrations of drug or PBO 8:2 per cohort COHORT 1: 2 mg/kg sabirnetug or Placebo 2mg COHORT 2: 10 mg/kg sabirnetug or Placebo 10mg COHORT 3: 25 mg/kg sabirnetug or Placebo 25mg COHORT 4: 60 mg/kg sabirnetug or Placebo 60mg COHORT 5: 10 mg/kg sabirnetug or Placebo (Q4W)* 10mg COHORT 6: 60 mg/kg sabirnetug or Placebo (Q4W)* 60mg COHORT 7: 25 mg/kg sabirnetug or Placebo (Q2W)* ≥ 1wk ≥ 1wk ≥ 1wk ≥ 1wk ≥ 1wk ≥ 1wk 25mg ≥ 1wk INTERCEPT-AD: A Randomized Placebo Controlled Phase 1 in Early AD Patients 13

Doses Approaching Maximal Target Engagement Support Sabirnetug AβO Mechanism and Helped Guide Dose Selection for Next Study Phase 14 Single & Multiple Dose Cohorts - Exposure Response Relationship (Emax Model) Emax: 22.71 AU/mL Complex EC50: 136 ng/mL sabirnetug 0 600 1200 1800 0 10 20 30 CSF [ACU193] (ng/mL) A C U 1 9 3 -A β O C o m p le x ( A U /m L ) SAD 2 mg/kg SAD 10 mg/kg SAD 25 mg/kg SAD 60 mg/kg MAD 10 mg/kg Q4W MAD 60 mg/kg Q4W MAD 25 mg/kg Q2W Sabirnetug-AO Complex TARGET ENGAGEMENT *One patient from Cohort 5 (10 mg/kg Q4W) excluded because only received one administration of drug (study drug discontinued after lacunar infarct). E. Siemers, et al. INTERCEPT-AD, a phase 1 study of intravenous sabirnetug in participants with mild cognitive impairment or mild dementia due to Alzheimer's disease. JPAD 2025. • Acumen developed a novel assay to measure the complex of AβOs bound to sabirnetug in cerebrospinal fluid • Observed target engagement with oligomers that increased across a range of doses • Achieved saturation point between 25 mg/kg and 60 mg/kg

Importance of Key Fluid Biomarkers Associated with AD Pathology 15 Tau Pathology: pTau181 pTau217 Neuronal Injury: Total tau Synaptic Injury: Neurogranin VAMP2 Amyloid Pathology: Aβ 42/40 Astrocytic Activation: GFAP • Biomarkers from cerebrospinal fluid and plasma capture neuronal, synaptic, and axonal injury and reflect the cumulative outcome of different pathological substrates in AD1 • Evidence suggests that biomarkers are likely to be better predictors of the underlying pathology of AD than imaging alone2 • After just three administrations of sabirnetug, patients with early AD demonstrated improvements in biomarkers associated with AD pathology 1. Tarawneh, R. Biomarkers: Our Path Towards a Cure for Alzheimer Disease. Biomarker Insights Volume 15: 1–15. 2020; 2. Blennow K, Zetterberg H. The Past and the Future of Alzheimer's Disease Fluid Biomarkers. J Alzheimer's Dis. 2018;62(3):1125-1140. A oligomer Amyloid plaque

Consistent Improvement in CSF Amyloid, Tau and Synaptic Biomarkers Indicate Downstream Pharmacology of Sabirnetug After Only Three Doses 16 CSF BIOMARKERS pTau181 NeurograninA 42/40 Ratio VAMP2 Tau pathologyAmyloid pathology Synaptic injury n = 8 subjects/treated group; 6 subjects in pooled placebo (PBO); p-values from unpaired, 2-sided Student’s t test N o rm a liza tio n A D P ro g re ssio n N o rm a liza tio n A D P ro g re ssio n N o rm a liza tio n A D P ro g re ssio n N o rm a liza tio n A D P ro g re ssio n E. Cline, et al, Biofluid biomarker changes following treatment with sabirnetug (ACU193) in INTERCEPT-AD, a phase 1 trial in early Alzheimer’s disease. JPAD 2025.

Sabirnetug Shows Greater or Similar Improvement in Multiple CSF Biomarkers as Compared to Other Aβ Agents 17 CSF BIOMARKERS CSF NeurograninCSF pTau181 50 100 -35 -25 -15 -5 5 15 Weeks C S F p T a u 1 8 1 (M e a n % c h a n g e f ro m b a s e li n e ) Gantenerumab (510 mg Q2W) Gantenerumab Placebo ACU193 (60 mg/kg Q4W) ACU193 (25 mg/kg Q2W) ACU193 (10 mg/kg Q4W) Pooled Placebo ACU193 Lecanemab (10 mg/kg Q2W) Lecanemab Placebo Trontinemab (3.6 mg/kg Q4W) C S F p T a u 1 8 1 (M e a n % c h a n g e f ro m b a s e li n e ) 50 100 -35 -25 -15 -5 5 15 Weeks C S F p T a u 1 8 1 (M e a n % c h a n g e f ro m b a s e li n e ) Gantenerumab (510 mg Q2W) Gantenerumab Placebo ACU193 (60 mg/kg Q4W) ACU193 (25 mg/kg Q2W) ACU193 (10 mg/kg Q4W) Pooled Placebo ACU193 Lecanemab (10 mg/kg Q2W) Lecanemab Placebo Trontinemab (3.6 mg/kg Q4W) 50 100 -35 -25 -15 -5 5 15 Weeks C S F p T a u 1 8 1 (M e a n % c h a n g e f ro m b a s e li n e ) Gantenerumab (510 mg Q2W) Gantenerumab Placebo ACU193 (60 mg/kg Q4W) ACU193 (25 mg/kg Q2W) ACU193 (10 mg/kg Q4W) Pooled Placebo ACU193 Lecanemab (10 mg/kg Q2W) Lecanemab Placebo Trontinemab (3.6 mg/kg Q4W) *There have been no head-to-head clinical trials between the product candidates listed above. Study designs and protocols for each product candidate were different, and as a result, results may not be comparable between product candidates. Acumen Pharmaceuticals, data on file; AAIC 2023; Bateman et al 2023 NEJM; ADPD 2025.

Sabirnetug Shows Greater or Similar Improvement in Plasma pTau217 Biomarker as Compared to Other Aβ Agents 18 PLASMA BIOMARKERS Plasma pTau217 *There have been no head-to-head clinical trials between the product candidates listed above. Study designs and protocols for each product candidate were different, and as a result, results may not be comparable between product candidates. Acumen Pharmaceuticals, data on file; AAIC 2023; Sims et al 2023 JAMA; ADPD 2025. Note: More impact to fluid biomarkers was observed with longer dosing duration; the 25 mg/kg Q2W cohort differed in dose and sample timing, with drug on board for less time than the 10 mg/kg & 60 mg/kg Q4W cohorts

Highest Doses of INTERCEPT-AD Reduced Amyloid Plaque at Similar Rate and Magnitude to Lecanemab at Comparable Timepoints 6% slowing of cognitive decline 8% slowing of cognitive decline -2% slowing of cognitive decline 22% slowing of cognitive decline 27% slowing of cognitive decline 23% slowing of cognitive decline 29% slowing of cognitive decline Efficacy achieved Mean reduction in amyloid plaque (centiloids)* Acumen Pharmaceuticals, data on file; van Dyck (2023), NEJM (amyloid PET reduction estimated from graphs). *There have been no head-to-head clinical trials between the product candidates listed above. Study designs and protocols for each product candidate were different, and as a result, results may not be comparable between product candidates. 19 PLAQUE REDUCTION

Sabirnetug Demonstrates Potential for Best-in-Class Safety Profile Compelling Overall Safety Profile, with Low Incidence of ARIA-E in the INTERCEPT-AD study 20 SAFETY ✓ Limited incidence of ARIA-E • 10 mg/kg Q4W: 1 asymptomatic case • 25 mg/kg Q2W: 1 asymptomatic case • 60 mg/kg Q4W: 2 asymptomatic cases; 1 symptomatic case ✓ No ARIA-E observed in ApoE4 homozygotes (n=6), despite comprising 13% of study • Differentiated from other antibodies that have ARIA-E rates ~30% to ~40% in participants who are E4-homozygotes ✓ Broad therapeutic index with convenient monthly dosing • Safety profile may support attractive benefit/risk option for large portion of patients 5 0 Total ARIA-E cases, or ~10% Cases of ARIA-E in ApoE4 homozygotes N=6 0 Deaths, SAEs Related to Study Drug INTERCEPT-AD Phase 1 Safety Data E. Siemers, et al. INTERCEPT-AD, a phase 1 study of intravenous sabirnetug in participants with mild cognitive impairment or mild dementia due to Alzheimer's disease. JPAD 2025. ApoE4: ε4 allele of Apolipoprotein E

Potential for Differentiated Efficacy Potential for Differentiated Safety INTERCEPT-AD Phase 1 Data Support Potential for Sabirnetug to Offer Next Generation Efficacy and Safety 21 ✓ Compelling safety profile with low incidence of ARIA-E ✓ Absence of ARIA-E observed in ApoE4 homozygotes ✓ Broad potential therapeutic index with convenient monthly dosing ✓ First mAb to demonstrate selective target engagement of AβOs (most toxic form of Aβ) ✓ Rapid, significant plaque reduction comparable to the current market front-runners at similar timepoints ✓ Improvement of AD biomarkers in CSF and plasma are a strong indication of downstream effects Key Takeaways from INTERCEPT-AD

R a n d o m iz a ti o n 1 :1 :1 Sabirnetug 35mg/kg Q4W (n ~180) Sabirnetug 50mg/kg Q4W* (n ~180) Placebo Q4W (n ~180) Primary Endpoint Change in iADRS1 at 18 months Secondary Endpoints1 CDR-SB, ADAS- Cog13, ADCS-ADL, AD biomarkers 12-month open label extension Objective: To evaluate the clinical efficacy, safety and tolerability of sabirnetug Patient population: Patients with early AD (MCI or mild dementia due to early AD) ALTITUDE-AD Phase 2 Study Results Expected in Late 2026 1. iADRS: Integrated Alzheimer's Disease Rating Scale; CDR-SB: Clinical Dementia Rating – Sum of Boxes; ADAS-cog: Alzheimer's Disease Assessment Scale – Cognitive Subscale; ADCS-ADL: Alzheimer's Disease Cooperative Study – Activities of Daily Living 22 *Titration of sabirnetug 35mg/kg Q4W for two doses. • 542-participant study fully enrolled in March 2025 (U.S., Canada, U.K., Germany, Spain) • Open label extension portion of ALTITUDE-AD initiated in November 2025 • Topline results expected in late 2026 Key Highlights

Subcutaneous Formulation Well-Tolerated in Phase 1 Healthy Volunteer Study Potential to Dose Once-Weekly with Single Injection to Broaden Patient Access and Increase Treatment Convenience Topline results announced in March 2025 show systemic exposure supports further clinical development of the subcutaneous formulation 23 Phase 1 study to compare the pharmacokinetics of subcutaneous form of sabirnetug to the IV form Outcomes: • Safety • Subcutaneous bioavailability • Information on flat dosing Population: • Healthy volunteers • Age matched to AD population in sabirnetug Phase 1 (INTERCEPT-AD) study IV dose (single dose) (n = 12) Subcutaneous dose (4 doses, 1/week) (n = 16) Phase 1 Subcutaneous Healthy Volunteer Study Announced partnership with Halozyme in November 2023 to develop subcutaneous dosing option for sabirnetug using Halozyme’s drug delivery technology, ENHANZE®

Sabirnetug IP & Market Exclusivity • Exclusive, perpetual, irrevocable, worldwide, royalty-free license from Merck to its Amyloid Derived Diffusible Ligand (ADDL) IP including issued sabirnetug patents • Sabirnetug Global IP estate: ✓ Issued patents in 19 countries ✓ Composition of matter patents and methods of use run into July 2031 ✓ Patent term extensions may be available, 3-5 years depending on jurisdiction • Biologics market exclusivity is expected for sabirnetug as a novel biologic drug ✓ US provides 12 years market exclusivity for novel biologics ✓ Europe provides 10 years of market exclusivity for novel biologics • EBDTM program includes Acumen wholly-owned AO-selective mAbs expected to generate novel IP including Composition of Matter Patent(s) 24

Enhanced Brain Delivery (EBDTM)

26 Delivering Antibodies to the Brain via the Transferrin Receptor (TfR) Aim to Widen the Therapeutic Window to Increase Efficacy, Safety, and Convenience • Increased brain exposure may enhance efficacy • Wider capillary distribution may reduce ARIA-E risk • Lower dose volumes enable convenient subcutaneous administration Enhanced Brain Delivery (EBD) Opportunities: Oligomer-targeted antibody TfR-targeted carrier ✓ Collaboration, option and license agreement announced in July 2025 with JCR Pharmaceuticals ✓ Acumen holds exclusive option to license and develop up to two candidates under terms of agreement Image courtesy of JCR Pharmaceuticals

Acumen's EBD May Improve Efficacy, Safety and Delivery Compared to Non-AβO Selective Antibodies Differentiated Cargo (AβO-selective mAb) 27 Differentiated Aβ targeting Validated TfR-binding Validated BBB Carrier Technology (TfR-targeting) Acumen EBD Candidates • Targets synaptotoxic A species • Robust fluid biomarker results in Phase 1b INTERCEPT-AD trial • Demonstrated low ARIA-E overall in Phase 1b, including no ARIA- E observed in APOE 4/4 carriers • Low rate of infusion related reactions observed to date clinically • Candidate mAbs: ACU193 and ACU234 • Enhance brain penetration versus native antibody to enable low- volume SC delivery • Potential for lower ARIA rate due to TfR prevalence on capillary bed • Little to no anemia observed with JCR technologies = Enhanced efficacy: Leverage improved brain delivery/ distribution and Aβ oligomer targeting Best-in-class safety: Lower ARIA, anemia, IRRs Designed for SC administration: Low dose, formulation, stability ApoE4: ε4 allele of Apolipoprotein E

Acumen Explored Broad Parameters to Develop a TfR-Mediated AβO Product 28 TfR Affinity Architecture Valency AβO Selectivity scFv or VHH Heavy Chain vs Light Chain Monovalent Bivalent Affinity Range Selectivity Range SQ Properties 14,000x 5,000x Dosing, Formulation, Stability TfR: transferrin receptor; scFv: single chain variable fragment antibodies; VHHs: variable heavy domain antibodies; SQ: subcutaneous

Multiple Dose Cohorts* Half-life/Dosing Interval Once monthly dosing Dosing Exposure 35 mg/kg and 50 mg/kg in Phase 2 IV Target Engagement Maximal TE of AβOs observed Phase 1 Results Provide Foundation for EBDTM Program 29 Single & Multiple Dose Cohorts - Exposure Response Relationship (Emax Model) Emax: 22.71 AU/mL Complex EC50: 136 ng/mL sabirnetug 0 600 1200 1800 0 10 20 30 CSF [ACU193] (ng/mL) A C U 1 9 3 -A β O C o m p le x ( A U /m L ) SAD 2 mg/kg SAD 10 mg/kg SAD 25 mg/kg SAD 60 mg/kg MAD 10 mg/kg Q4W MAD 60 mg/kg Q4W MAD 25 mg/kg Q2W *One patient from Cohort 5 (10 mg/kg Q4W) excluded because only received one administration of drug (study drug discontinued after lacunar infarct). E. Siemers, et al. INTERCEPT-AD, a phase 1 study of intravenous sabirnetug in participants with mild cognitive impairment or mild dementia due to Alzheimer's disease. JPAD 2025.

Mouse Surrogate Antibodies Developed to Explore EBDTM and Target Engagement in a Mouse Model of Alzheimer’s Disease 30 The fusion of anti-oligomer antibodies and J-Brain Cargo (anti-TfR scFv) did not alter the ability of constructs to bind TfR or alter the preferential binding to AβOs Cline et al., CTAD, 2025 234 0 nM Oligomer Binding Monomer Binding 2.182 nM 3.761 M ACU193 0.33 nM 5.34 nM 3.52 nM 0.595 nM 0.448 nM 2.475 nM 6.914 M 5.871 M 8.6 M mTfR: murine transferrin receptor; mscFv: murine single chain variable fragment antibodies 0.319 * *Cline et al., AAIC, 2025

Animals dosed IV at 2 mpk Cline et al., CTAD, 2025 • Higher brain exposure was observed for all fusion proteins compared to ACU193: o mBBB.193-1 exhibited ~35-fold higher brain exposure at 3 hours o mBBB.193-2 and mBBB.234-2 exhibited ~17-fold higher brain exposure at 24 hours • mBBB.193-2 and mBBB.234-2 showed the greatest cumulative exposure: o 32- to 55-fold higher AUC than ACU193 In Wild-Type Mice, All EBDTM Fusion Proteins Showed Increased Brain Exposure Compared to Sabirnetug (ACU193) ~ 35x @ 3 hrs ~ 17x @ 24 hrs 31

Surrogate Antibodies Show Enhanced Delivery to the AD Mouse Brain, when Compared with ACU193 and ACU234 AD Mouse Model (ATRE10) Animals dosed at IV 2 mpk Cline et al., CTAD, 2025 ~ 63X ~ 68X ~ 65X 32 • The brain exposure of the three fusion proteins was 63- to 68-fold higher compared to ACU193 and ACU234 • Higher concentrations of all three fusion proteins seen in AD mouse brain compared to wild-type mice may be due to target engagement of AβOs and retention in brain

Robust Data Package Supporting EBDTM Construct Selection Inclusive of NHP Primate Data Anemia Risk Brain Distribution Stability & Manufacturability Pharmacokinetics TfR Affinity 33 Aβ Oligomer Binding

Key Takeaways from NHP Study Results 34 ✓ Enhanced Brain Penetration EBD candidates achieved 14-40x higher brain levels in non-human primates compared to native antibodies 24 hours after dosing Lead clinical candidate IND targeted for 2027 ✓ Subcutaneous Dosing Capability Favorable stability profile and enhanced brain delivery support a path to subcutaneous administration with low-volume devices ✓ Low Anemia Risk • Hematology data in non-human primates indicate low potential for anemia: At 24 hours after SC dosing, EBD candidates demonstrated no observed change in red blood cell count, hematocrit, hemoglobin or reticulocyte count • No adverse events observed

✓ Significant and growing Alzheimer’s population in need of additional treatment options ✓ Synaptotoxic AβOs appear early in Alzheimer’s Disease and contribute to its pathophysiological processes; sabirnetug demonstrates high selectivity for AβOs in AD patients ✓ Positive Phase 1 data strengthen potential for sabirnetug to offer next-generation efficacy and safety ✓ Significant interest in ALTITUDE-AD, a Phase 2 study investigating sabirnetug, evidenced by rapid enrollment ✓ Enhanced Brain DeliveryTM program augments portfolio optionality, leveraging Acumen capabilities and assets Acumen Positioned to Deliver Potential Next-Gen Treatment for Early AD 35 Key Takeaways Next Steps ✓ EBDTM program pre-clinical candidate (PCC) data announced in early 2026 ❑ Topline results from ALTITUDE-AD Phase 2 IV study evaluating the clinical efficacy and safety of sabirnetug in patients with MCI or mild dementia due to Alzheimer’s expected in late 2026 ❑ IND for EBD program targeted for mid-2027

Appendix www.acumenpharm.com 36

Current Anti-A Antibodies in Preclinical/Clinical Development or Launched O li g o m e rs Target Preclinical Phase 1 Phase 2 Phase 3 Launched Sabirnetug Acumen PMN310 ProMIS CM383 KeyMed Trontinemab Roche Leqembi Eisai/Biogen Kisunla Lilly Remternetug Lilly ALIA-1758 AbbVie TAPAS LifeArc ILM-01 Illimis ABY1125 Abyssinia AβO TfR EBD Acumen/JCR ALZ-201 Alzinova morADC AC Immune DNL921 Denali ATV:Abeta Denali BAN2802 Eisai/Bioarctic SNP234 SciNeuro BAN1503 Bioarctic AL137 Alector AL037 Alector Eisai/Bioarctic PRX012 TfR Prothena BAN2803 BMS/Bioarctic TfR Brain deliveryAlector CD98 Brain delivery TfR: Transferrin receptor; CD98: Cluster of differentiation 98; Adapted from DeMattos, R., CTAD 2025. F ib ri ls N 3 p G U n sp e ci fi e d SHR-1707 Hengrui NI-10183 Neurimmune No Brain delivery P ro to - F ib ri ls KRSA-028 Korsana 37

Non-clinical Sabirnetug Data

Amyloid Beta Oligomers (AβOs) in Alzheimer’s Disease Pathology Aβ monomers are normally produced, non- toxic and orders of magnitude more prevalent than other forms of amyloid. Aβ plaques are relatively inert but serve as reservoirs for toxic species of amyloid: oligomers and protofibrils. Neurotoxic Soluble Amyloid Insoluble Amyloid

Literature Selection: Soluble AβOs Contribute to Pathophysiological Processes Associated with Alzheimer’s Disease Disrupted Ca2+ homeostasis Demuro et al, 2005 De Felice et al, 2007 Alberdi et al, 2010 Wang et al, 2018 ChAT loss Heinitz et al, 2006 Nunes-Tavares et al, 2012 Inhibition of axonal transport Pigino et al, 2009 Poon et al, 2009 Decker et al, 2010 Oxidative stress Longo et al, 2000 Sponne et al, 2003 Tabner et al, 2005 De Felice et al, 2007 ER stress Resende et al, 2008 Nishitsuji et al, 2009 Insulin resistance Zhao et al, 2008 Zhao et al, 2009 Ma et al, 2009 De Felice et al, 2009 Impact on astrocytes/microglia Hu et al, 1998 Jimenez et al, 2008 Sondag et al, 2009 Tomiyama et al, 2010 Aberrant Tau phosphorylation De Felice et al, 2008 Ma et al, 2009 Tomiyama et al, 2010 Zempel et al, 2010 Bloom, 2014 Forny-Germano et al, 2020 Wakeman et al, 2022 Darricau et al, 2023 Selective neuron death Lambert et al, 1998 Kim et al, 2003 Florent et al, 2006 Ryan et al, 2009 Lee et al, 2017 Komura, 2019 Plasticity dysfunction Lambert et al, 1998 Walsh et al, 2002 Wang et al, 2002 Townsend et al, 2006 Yasumoto et al, 2019 Synapse deterioration Zhao et al, 2006 Lacor et al, 2007 Shankar et al, 2007 Wu et al, 2010 Brito-Moreira et al, 2017 Actor-Engel et al, 2021 Sackmann & Hallbeck, 2020 Limegrover et al, 2021 Receptor Redistribution Snyder et al, 2005 Roselli et al, 2005 Lacor et al, 2007 Zhao et al, 2008 40

• Aβ monomers are ~7000x higher concentration than AβOs in AD CSF • Higher affinity for monomeric Aβ will reduce functional selectivity due to high monomer levels • Sabirnetug has much lower affinity than other mAbs for Aβ monomers Sabirnetug Demonstrates Low Affinity for Monomeric Aβ 41 M urin e D onan em ab A duca num ab Lec an em ab S ab irn et ug 0 2×10 -6 4×10 -6 6×10 -6 Aβ1-40 monomer binding A ff in it y - K D ( M ) 100.2 nM 338.2 nM 215.7 nM 5215.5 nM H ig h e r b in d in g a ff in it y Internal data, 2024 Note: Calculated KD value for sabirnetug was above the highest analyzed concentration.

Sabirnetug is Highly Selective for Aβ Oligomers Versus Aβ Monomers Relative Selectivity for AβO versus Monomeric Aβ Measured with SPR 42 Sabirnetug is more selective for AβOs than aducanumab or lecanemab Aducanumab Lecanemab Sabirnetug 1×10 -10 1×10 -9 1×10 -8 1×10 -7 1×10 -6 1×10 -5 Sabirnetug vs Lecanemab and Aducanumab A ff in it y - K D ( M ) Aβ1-40 monomer Aβ oligomers 8750x 222x 79.6x H ig h e r b in d in g a ff in it y Internal data, 2024 Note: Murine donanemab shows very low signals for Aβ oligomer binding compared to all other antibodies tested; therefore, it was not included in this comparison.

43 AD Hippocampus ThioS/amyloid plaque AD Hippocampus ACU193/AOs species Sabirnetug is Selective for AβOs Versus Aβ Plaques Sabirnetug Thioflavin S Sabirnetug Binds AβOs Not Associated with Plaques in Human AD Brain Slices Adapted from Krafft et al. 2022

44 Amyloid Plaques are Surrounded by a Halo of AβOs Transgenic mouse model of AD AβOs can form halos of soluble aggregates around dense core of amyloid plaques, to which sabirnetug also binds Sabirnetug binding to soluble AβOs Sabirnetug Plaque (ThioS) Spires-Jones et al. 2014 AOs (AW7) Plaque (ThioS) AD human brain tissue Lab of William Klein, NU, 2017

Sabirnetug: Extensive Data Package Supporting Development Sabirnetug is a promising immunotherapy for early AD expected to provide meaningful cognitive and functional benefits, slow disease progression, and offer an attractive safety profile  Nanomolar affinity for AβOs, >500-fold greater selectivity for AβOs over Aβ monomer, with limited or no discernable binding to vascular amyloid or dense core amyloid plaques  Binds broad range of endogenous Aβ, from dimers to high molecular weight AβOs  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  IgG2 subclass lacks inflammatory effector function signaling (FcγR binding)  Non-clinical microhemorrhage studies show no increased risk of microhemorrhage  GLP studies demonstrated acceptable safety package supporting clinical dosing plans including Phase 2 SELECTIVITY PHARMACOLOGY PK/PD SAFETY 45

Highly selective for Aβ oligomers versus Aβ monomers Even in the presence of a large excess of Aβ monomer, binding of sabirnetug to AβOs is unchanged Binding of sabirnetug to AβOs >500x binding to Aβ monomer Log [Competing Antigen] μM Sabirnetug Selectivity Sabirnetug Selectivity in presence of 5μM monomeric Aβ ACU193 Log μM Sabirnetug is the First mAb Developed to Selectively Target AβOs Sabirnetug selective for binding to AβOs is preserved even in the presence of a large excess of Aβ monomers – such as what is present in the brain, thus limiting ‘target distraction’ 46

47 Sabirnetug Recognizes a Wide Range of Oligomeric Species of Aβ Broad AβO size distribution recognized by sabirnetug in human AD brain Sabirnetug dose dependently binds to AβOs in brain tissue from Tg2576 mice Data from lab of William Klein, NU, 2018 Merck internal data, 2011 0 0.2 0.4 0.6 0.8 1 1.2 1101001000 R e la ti v e A β O Im m u n o re a ct iv it y w it h S a b ir n e tu g Molecular Weight (kDa) ~3-8 mers~18-100 mers

1. Prevention of hippocampal LTP impairment Functional Consequences of AβO Clearance: Restoring Plasticity 48 • Aβ at 50 nM markedly reduced HFS-induced LTP in wildtype slices • Pre-treatment with ACU3B3 oligomer-selective antibody prevented Aβ1-42-induced LTP deficits Time course of LTP induction From manuscript in prep; data collected by lab of Gerhard Rammes, University of Regensburg, Max-Planck Institute of Psychiatry, Germany

Functional Consequences Following ACU3B3 Treatment 49 • ACU3B3 (murine oligomer selective antibody) treatment prior to plaque pathology leads to reduced amyloid deposition in J20 Tg model (5-7 months) • Treatment effects are less prominent in aged animals (16-23 months) • Evidence of synaptic recovery in advanced stages of pathology in contrast to minor effects on plaque deposition From manuscript in prep; data collected by lab of Jorge Palop, Gladstone Institute 2. Reduced amyloid deposition and increased spine density

Phase 1 INTERCEPT-AD

Sabirnetug drug specific capture (anti-sabirnetug idiotype mAb) 51 Target Engagement Assessed by Measuring Sabirnetug-AO Complex in CSF AO selective detection (anti-A mAb) Only Sabirnetug-AO complex is measurable • Novel assay configuration tailored to selectively detect sabirnetug-AβO complex in CSF as direct measure of target engagement • Translated for clinical use from a preclinical assay developed by Merck that showed sabirnetug engages target AβOs in transgenic mouse brain (tg2576) in dose dependent manner MSD S-Plex (Turbo) Immunoassay TARGET ENGAGEMENT

Target Engagement of Sabirnetug with AβOs is Dose Proportional 52 Single Dose Cohorts Multiple Dose Cohorts* 2 mg/kg 10 mg/kg 25 mg/kg 60 mg/kg 0 10 20 30 ACU193 IV Infusion Dose C S F A C U 1 9 3 -A β O li g o m e r C o m p le x ( A U /m L ) a t V is it 8 ( D a y 2 1 ) *One patient from Cohort 5 (10 mg/kg Q4W) excluded because only received one administration of drug (study drug discontinued after lacunar infarct). TARGET ENGAGEMENT p = 0.001 p = 0.03 p = 0.0007No Significant Differences E. Siemers, et al. INTERCEPT-AD, a phase 1 study of intravenous sabirnetug in participants with mild cognitive impairment or mild dementia due to Alzheimer's disease. JPAD 2025.

Nearly All Sabirnetug-Treated Patients in High Dose MAD Cohorts Showed Reductions in Plaque Load After Three Doses at 63 or 70 days 53 Plaque load based on florbetapir PET 0 15 30 45 60 75 0 25 50 75 100 125 25 mg/kg Q2W MAD Days C e n ti lo id s 20 21 22 23 24 25 26 27 0 15 30 45 60 75 0 25 50 75 100 125 60 mg/kg Q4W MAD Days C e n ti lo id s 28 29 30 31 32 33 34 35 25 mg/kg Q2W MAD 60 mg/kg Q4W MAD Mean reduction in amyloid plaque ∆ (absolute value, centiloids) 13.7 ∆ (%, centiloids) 20.6% Mean reduction in amyloid plaque ∆ (absolute value, centiloids) 18.1 ∆ (%, centiloids) 25.6% PLAQUE REDUCTION E. Siemers, et al. INTERCEPT-AD, a phase 1 study of intravenous sabirnetug in participants with mild cognitive impairment or mild dementia due to Alzheimer's disease. JPAD 2025.

Sabirnetug Serum Exposure is Dose Proportional Without Accumulation 54 Single Dose Cohorts Multiple Dose Cohorts PHARMACOKINETICS Estimated serum terminal T1/2 of 5-7 days E. Siemers, et al. INTERCEPT-AD, a phase 1 study of intravenous sabirnetug in participants with mild cognitive impairment or mild dementia due to Alzheimer's disease. JPAD 2025.

Sabirnetug CSF Exposure is Dose and Dose-Regimen Proportional 55 Single Dose Cohorts Multiple Dose Cohorts* *One patient from Cohort 5 (10 mg/kg Q4W) excluded because only received one administration of drug (study drug discontinued after lacunar infarct). PHARMACOKINETICS E. Siemers, et al. INTERCEPT-AD, a phase 1 study of intravenous sabirnetug in participants with mild cognitive impairment or mild dementia due to Alzheimer's disease. JPAD 2025.

Trend Toward Normalizing Plasma Biomarkers with 10 mg/kg and 60 mg/kg Q4W 56 M A D P B O 10 m g/k g Q 4W 25 m g/k g Q 2W 60 m g/k g Q 4W -100 -50 0 50 100 150 P la s m a G F A P (% c h a n g e f ro m b a s e li n e ) M A D P B O 10 m g/k g Q 4W 25 m g/k g Q 2W 60 m g/k g Q 4W -50 0 50 100 P la s m a p T a u 1 8 1 (% c h a n g e f ro m b a s e li n e ) M A D P B O 10 m g/k g Q 4W 25 m g/k g Q 2W 60 m g/k g Q 4W -100 -50 0 50 100 150 P la s m a p T a u 2 1 7 (% c h a n g e f ro m b a s e li n e ) 1 -6 w k p o st -d o si n g • Plasma measurements of glial fibrillary acidic protein (GFAP), pTau181, and pTau217 in 10 mg/kg Q4W & 60 mg/kg Q4W groups were lower than placebo • More impact to fluid biomarkers was observed with longer dosing duration o The 25 mg/kg Q2W cohort differed in dose and sample timing, with drug on board for less time than the 10 mg/kg & 60 mg/kg Q4W cohorts PLASMA BIOMARKERS pTau181GFAP pTau217 A D P ro g re ssio n N o rm a liz a tio n n = 8 subjects/treated group; 6 subjects in pooled placebo (PBO); p-values from unpaired, 2-sided Student’s t test E. Cline, et al, Biofluid biomarker changes following treatment with sabirnetug (ACU193) in INTERCEPT-AD, a phase 1 trial in early Alzheimer’s disease. JPAD 2025.

Phase 2 ALTITUDE-AD

Simulated CSF Target Engagement at Steady-State for ALTITUDE-AD Doses • CSF target engagement was simulated at a candidate list of doses given Q4W at steady-state • Notable diminishing differentiation as dose increases • Doses were selected with peak-trough variation in mind: select doses based on trough (end of dosing interval) CSF engagement upper dose: 50 mg/kg Q4W lower dose: 35 mg/kg Q4W Ph2 Dosing Strategy (ALTITUDE-AD) TIME 58

FAQ

What did Acumen Pharmaceuticals (ABOS) announce in its latest 8-K filing?

Acumen Pharmaceuticals announced a private placement of common stock raising approximately $35.75 million. The company agreed to sell 10,833,331 shares at $3.30 per share to institutional and accredited investors, with closing expected on March 16, 2026, subject to customary conditions.

How will Acumen Pharmaceuticals (ABOS) use the $35.75 million private placement proceeds?

The company plans to use net proceeds primarily to support its Enhanced Brain Delivery (EBD™) program. This includes ongoing preclinical development to select a lead clinical candidate, as well as working capital and other general corporate purposes tied to its Alzheimer’s-focused pipeline.

What are the key terms of Acumen Pharmaceuticals’ (ABOS) private placement?

Acumen agreed to sell 10,833,331 common shares at an offering price of $3.30 per share, for expected gross proceeds of about $35.75 million. The securities are being issued in a private transaction relying on Section 4(a)(2) of the Securities Act, without immediate registration.

What registration rights did investors receive in the Acumen Pharmaceuticals (ABOS) financing?

Investors received a Registration Rights Agreement requiring Acumen to file a resale registration statement for the new shares shortly after its Form 10‑K for fiscal 2025. The company must use reasonable best efforts to have it declared effective and keep it effective until resale conditions are met.

Does the Acumen Pharmaceuticals (ABOS) 8-K mention any lock-up or issuance restrictions?

Yes. Under the Securities Purchase Agreement, Acumen agreed to certain restrictions on issuing and selling additional securities from signing until the earlier of sixty days after closing or the business day after the resale registration statement becomes effective, subject to specified exceptions.

How does the private placement relate to Acumen Pharmaceuticals’ Enhanced Brain Delivery (EBD) program?

The company explicitly states that proceeds are primarily intended to support its EBD™ program. This includes preclinical work backing transferrin-receptor–targeted candidates, which have shown elevated brain exposure in non-human primates and are aimed at developing a lead clinical candidate.

What additional disclosures accompanied the Acumen Pharmaceuticals (ABOS) financing announcement?

Acumen also released a press release and updated corporate presentation on March 16, 2026. These materials highlighted preclinical EBD program data, including in vitro, in vivo and non-human primate results, and reiterated an investigational new drug (IND) submission target around mid‑2027.

Filing Exhibits & Attachments

7 documents

Press Releases

• EX-99.1 EX-99.1 29.3 KB
• EX-99.2 EX-99.2 56.4 KB

Agreements & Contracts

• EX-10.1 EX-10.1 243.3 KB
• EX-10.2 EX-10.2 147.6 KB

Other Documents

• EX-101 XBRL TAXONOMY EXTENSION SCHEMA DOCUMENT 1.7 KB
• EX-101 XBRL TAXONOMY EXTENSION LABEL LINKBASE DOCUMENT 22.9 KB
• EX-101 XBRL TAXONOMY EXTENSION PRESENTATION LINKBASE DOCUMENT 13.3 KB