Forward Looking Statement This presentation contains "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995, including statements regarding future expectations, plans and

42nd Annual J.P. Morgan Healthcare

Conference January 2024 Exhibit 99.1

Forward Looking Statement This

presentation contains "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995, including statements regarding future expectations, plans and prospects for the company; the ability to

successfully achieve and execute on the company's priorities and achieve key preclinical and clinical milestones; the company's plans with respect to its Phase 1/2 clinical trial for SGT-003; the company's plans for filing an IND

for SGT-501; the company's preclinical programs, including expectations for filing INDs, and the company's future development of preclinical and capsid programs; and other statements containing the words "anticipate,"

"believe," "continue," "could," "estimate," "expect," "intend," "may," "plan," "potential," "predict," "project,"

"should," "target," "would," "working" and similar expressions. Any forward-looking statements are based on management's current expectations of future events and are subject to a number of risks

and uncertainties that could cause actual results to differ materially and adversely from those set forth in, or implied by, such forward-looking statements. These risks and uncertainties include, but are not limited to, risks associated with the

ability to recognize the anticipated benefits of Solid's acquisition of AavantiBio; the company's ability to advance SGT-003, SGT-501, AVB-401, AVB-202-TT and other preclinical programs and capsid libraries on the timelines expected or

at all; obtain and maintain necessary approvals from the FDA and other regulatory authorities; replicate in clinical trials positive results found in preclinical studies of the company's product candidates; obtain, maintain or protect

intellectual property rights related to its product candidates; compete successfully with other companies that are seeking to develop Duchenne and other neuromuscular and cardiac treatments and gene therapies; manage expenses; and raise the

substantial additional capital needed, on the timeline necessary, to continue development of SGT-003, SGT-501, AVB-401, AVB-202-TT and other candidates, achieve its other business objectives and continue as a going concern. For a discussion of other

risks and uncertainties, and other important factors, any of which could cause the company's actual results to differ from those contained in the forward-looking statements, see the "Risk Factors" section, as well as discussions of

potential risks, uncertainties and other important factors, in the company's most recent filings with the Securities and Exchange Commission. In addition, the forward-looking statements included in this presentation represent the

company's views as of the date hereof and should not be relied upon as representing the company's views as of any date subsequent to the date hereof. The company anticipates that subsequent events and developments will cause the

company's views to change. However, while the company may elect to update these forward-looking statements at some point in the future, the company specifically disclaims any obligation to do so. This presentation contains estimates and other

statistical data made by independent parties and by us relating to market size and other data about our industry. This data involves a number of assumptions and limitations, and you are cautioned not to give undue weight to such data and estimates.

In addition, projections, assumptions and estimates of our future performance and the future performance of the markets in which we operate are necessarily subject to a high degree of uncertainty and risk.

Diversified Pipeline Strategic

Pipeline Across Multiple Therapeutic Areas Leading Collaborators Leading Edge CMC Capabilities Next Generation DMD Program New Management Team Industry Leading Platform, Partners, Pipeline, Management, and Strong Balance Sheet $123.9M* as of

12/31/23 & $100.0M+ In anticipated net proceeds from PIPE announced 1/8/2024 *Estimated cash, cash equivalents and available for sale securities figure is preliminary and unaudited, represents a management estimate as of the date of this

presentation and is subject to completion of our financial closing procedures

Program Indication Research /

Discovery Preclinical Phase 1/2 Milestone (anticipated) Worldwide Rights Neuromuscular SGT-003 Duchenne Initial FIH Data Q3 2024 AVB-202 - TT Friedreich's Ataxia Cardiac SGT-501 RYR2-Mediated CPVT IND Q1 2025 CASQ2-Mediated CPVT AVB-401

BAG3-Mediated DCM SGT-601 TNNT2 DCM SGT-701 RBM20 Platform Capsid Library* FIH Data Q3 2024** Clinical Stage Company With Additional Cardiac IND in Early 2025 Notes: In 2020, Solid entered into a collaboration agreement with Ultragenyx for the

development of UX810, a next generation Duchenne construct comprised of Solid's proprietary nNOS microdystrophin and Ultragenyx's HeLa PCL manufacturing platform for use with AAV8 and Clade E variants thereof. Solid has the option to

co-fund collaboration programs in return for a profit share or increased royalty payments at proof-of-concept. * Capsid Library currently in NHPs, Mice and Pigs, ** AAV-SLB101

Next-generation Construct Has Shown

Promising Results in Preclinical Testing Capsid Rational design approach used to engineer capsid candidates with the goal of improving skeletal muscle tropism Fold Change Dys Expression vs. AAV9 AAV9 AAV-SLB101 3.0 2.0 1.0 0.0 Robust Dys

Expression in mdx Mouse Transgene Solid's microdystrophin uniquely includes the nNOS binding domain, potentially important for prevention of activity-induced ischemia and associated muscle injury NH3 Hinge 1 4 Hinge COOH Actin

Binding Domain Dystroglycan Binding Domain nNOS Binding Domain R1 R16 R17 R23 R24 Manufacturing Process Current yields and empty to full ratios have potential to significantly reduce COGs for DMD and other gene therapies SGT-003 Utilizes an

Optimized Transgene, Next Generation Capsid and Improved Manufacturing Process Starting process Improvement 1 Improvement 2 Improvement 3 Improvement 4 2x 3x 1.5x 1.5x Empty/Full and Yield Improvements Full Capsids Empty Capsids

Quadriceps - Day 4 h-uD5+

Myofibers (%) 0 50 150 100 Vehicle SGT-003 3.0E13 SGT-003 1.0E14 SGT-003 3.0E14 Heart - Day 4 h-uD5+ Myofibers (%) 0 50 100 150 Vehicle SGT-003 3.0E13 SGT-003 1.0E14 SGT-003 3.0E14 Diaphragm - Day 4 h-uD5+ Myofibers (%) 0 50 100 150

Vehicle SGT-003 3.0E13 SGT-003 1.0E14 SGT-003 3.0E14 Rapid AAV-SLB101 Transduction and Expression in mdx Mouse Model by Day 4 N=5 per group Observations Robust microdystrophin expression levels, as assessed by h-uDys5+ myofibers in heart,

quadriceps, and diaphragm, were evident by Day 4 post-AAV-SLB101 administration

SGT-003 Showed Sustained

Microdystrophin Expression in mdx Mouse Muscle Vehicle 3.0E13 vg/kg 1.0E14 vg/kg 3.0E14 vg/kg % uDys5 Positive Fibers % uDys5 Positive Fibers Diaphragm 0 29 92 4 0 50 100 Days Post Dosing % uDys5 Positive Fibers Gastrocnemius 0 29 92 4 0 50 100 Days

Post Dosing % uDys5 Positive Fibers Tongue 0 29 92 4 0 50 100 Days Post Dosing Tibialis Anterior 0 29 92 4 0 50 100 Days Post Dosing % uDys5 Positive Fibers Quadriceps 0 29 92 4 0 50 100 Days Post Dosing % uDys5 Positive Fibers Heart 0 50 100 0 29

92 4 Days Post Dosing N=5 per group

High Microdystrophin Expression and

nNOS Activity in Multiple Tissues at Low Doses in mdx Mouse Model N=10 per group Microdystrophin Diaphragm % Positive Fibers 0 50 100 Quadriceps % Positive Fibers 0 50 100 Heart % Positive Fibers 0 50 100 WT Vehicle mdx Vehicle mdx SGT-003 (2.0E12)

mdx SGT-003 (6.0E12) mdx SGT-003 (3.0E13) WT Vehicle mdx Vehicle mdx SGT-003 (2.0E12) mdx SGT-003 (6.0E12) mdx SGT-003 (3.0E13) WT Vehicle mdx Vehicle mdx SGT-003 (2.0E12) mdx SGT-003 (6.0E12) mdx SGT-003 (3.0E13) Diaphragm nNOS Activity (%) 0 50

100 Quadriceps nNOS Activity (%) 0 50 100 WT Vehicle mdx Vehicle mdx SGT-003 (2.0E12) mdx SGT-003 (6.0E12) mdx SGT-003 (3.0E13) WT Vehicle mdx Vehicle mdx SGT-003 (2.0E12) mdx SGT-003 (6.0E12) mdx SGT-003 (3.0E13) nNOS Activity

Robust Dys Expression

in mdx Mouse Reduced CK Levels in mdx Mouse Tissue Specific Biodistribution in mdx Mouse 0 2 4 6 8 10 Quad Diaphragm Liver AAV9 Fold Change Dys vg/ g DNA vs. AAV9 Fold Change Dys Expression vs. AAV9 CK Level (U/L) 1 AAV9

AAV-SLB101 0 1000 mdx Vehicle mdx AAV9 mdx AAV-SLB101 WT Vehicle 2000 3000 4000 2 0 3 Serum CK (D29) SGT-003 With AAV-SLB101 Capsid Demonstrated Superior Muscle Tropism vs AAV9 Positive Biodistribution and Expression Data Has the Potential to

Translate Into Better Efficacy N=5 per group

Significant Microdystrophin

Expression and Functional Efficacy Observed in mdx Mouse Model at Low Doses (3E13) **p<0.005, ***p<0.0005, ****p<0.00005 N=10 per group Mass Spectrometry - % Normal Dystrophin Grip Strength (11 weeks) 0 1 2 3 4 5 Normalized Forelimb

(KgF/kg) ** *** ** WT Vehicle mdx Vehicle mdx SGT-003 (2.0E12) mdx SGT-003 (6.0E12) mdx SGT-003 (3.0E13) Quadriceps Heart Diaphragm 0 100 200 300 % Normal Dystrophin **** **** **** 0 100 200 300 **** **** **** ** 0 **** **** **** 100 200 300 %

Normal Dystrophin % Normal Dystrophin WT Vehicle mdx Vehicle mdx SGT-003 (2.0E12) mdx SGT-003 (6.0E12) mdx SGT-003 (3.0E13) WT Vehicle mdx Vehicle mdx SGT-003 (2.0E12) mdx SGT-003 (6.0E12) mdx SGT-003 (3.0E13) WT Vehicle mdx Vehicle mdx SGT-003

(2.0E12) mdx SGT-003 (6.0E12) mdx SGT-003 (3.0E13)

NHP IV Administration of AAV-SLB101

with Constitutive Promoter and Reporter Gene BIODISTRIBUTION NHPs Administered AAV-SLB101 Showed Improved Biodistribution in Cardiac and Skeletal Muscle With Decreased Hepatic Transduction as Compared to AAV9 *Average fold differences

calculated from the five skeletal muscle tissues sampled, three regions of cardiac tissue sampled, and the single liver sample. Dose 5e12 vg/kg N=2 per group Fold vs. AAV9 AAV9 AAV-SLB101 4.0 3.0 2.0 1.0 0.0 Liver Fold vs. AAV9 AAV9 AAV-SLB101 4.0

3.0 2.0 1.0 0.0 Cardiac Muscle Fold vs. AAV9 AAV9 AAV-SLB101 4.0 3.0 2.0 1.0 0.0 Skeletal Muscle Increased biodistribution to skeletal & cardiac muscle resulted in increased transgene expression* Reduced biodistribution in liver suggests tissue

de-targeting and potentially improved safety profile*

GLP Toxicology NHP Study Showed

SGT-003 Was Well Tolerated NHP GLP TOX Study 3-month study 2 treatment groups (1E14 vg/kg & 3E14 vg/kg) n = 3/group > 60 tissues evaluated including skeletal muscle, liver, brain Well tolerated in both groups throughout the study No early

mortality events, no unscheduled take downs No pathology findings: organ weight changes, macroscopic, or microscopic Liver enzyme levels comparable to vehicle at target clinical dose NHPs dosed at 3x planned first-in-human dose (1E14 vg/kg) FINDINGS

To investigate the safety and

tolerability of a single intravenous 1E14vg/kg dose of SGT-003 To investigate the efficacy of a single intravenous dose of SGT-003 Objective Design Endpoint First-in-human Open-label, Single-dose Study to Enroll a Minimum of 3 Patients From Two

Sites Primary Objective Secondary Objective FDA Cleared SGT-003 Phase 1/2 Trial Design

Study will include 2 cohorts based

on age, weight, and North Star Ambulatory Assessment (NSAA) at the time of signing the informed consent: Cohort 1: Participants 4 to < 6 years of age, <18 kg, NSAA total score 17 to <27 Cohort 2: Participants 6 to < 8 years of

age, <30 kg, NSAA total score 20 to <29 All participants will be required to be on a stable dose of at least 0.5 mg/kg/day of oral daily prednisone or 0.75 mg/kg/day deflazacort for 12 weeks prior to entering the study All

participants must be ambulant and have a diagnosis of DMD with a documented dystrophin gene mutation confirmed by genetic testing at screening. First-in-human Open-label, Single-dose Study to Enroll a Minimum of 3 Patients From Two Sites Objective

Design Endpoint Design FDA Cleared SGT-003 Phase 1/2 Trial Design

Primary Endpoint Secondary Endpoint

Incidence of treatment-emergent adverse events (AEs) through Day 360 Change from baseline of microdystrophin protein levels at Day 90 and 360 Change from baseline in the NSAA score at Day 360 Change from baseline in 6 minute walk

test (6MWT) distance at Day 360 Objective Design Endpoint First-in-human Open-label, Single-dose Study to Enroll a Minimum of 3 Patients From Two Sites FDA Cleared SGT-003 Phase 1/2 Trial Design

CASQ2 & RYR2 proteins regulate

cardiac calcium (Ca2+ ), important for electrical conduction and cardiac contraction / relaxation Postulated Mechanism: Mutations in RYR2 or CASQ2 genes disrupt Ca2+ release into the cytoplasm triggering abnormal contraction and

relaxation leading to arrythmias Cause Affected Population PREVALENCE 1:10,000 people1 AAV-delivered, CASQ2 transgene with cardiac-specific promoter designed for safe expression utilizing optimized transient transfection manufacturing process Solid

Approach ESTIMATED ~33,000 patients in the US Clinical Presentation and Unmet Need SIGNS & SYMPTOMS Quality of life severely impacted. Risk of spontaneous arrhythmias and or sudden death Poor Prognosis: ~40% mortality within 10 years of

diagnosis2 AGE OF ONSET Typically identified in younger patients (mean onset between 7-12 y/o) STANDARD OF CARE No available targeted therapies to address underlying disease cause CPVT Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT); a

Fatal Disorder in a Young Population RYR2=Ryanodine receptor, CASQ2= Calsequestrin 2 1. Napolitano et al, 2022 2. Sumitomo, 2016

Rationale for CASQ2 Overexpression

in RYR2 CPVT CASQ2 Overexpression Leads to Increased Ca2+ Buffering to Counteract Ca2+ Sensitivity of RYR2 Mutant RYR2 Mutation-related CPVT Mutations in RYR2 make the channel more sensitive to SR Ca2+ levels, resulting in early release of Ca2+ into

the cytoplasm and the heart contracting when it should be filling with blood in diastole CASQ2 Ca2+ CASQ2 Ca2+ CASQ2 RYR2 mutations lower threshold for SR Ca2+ release SR Free Ca2+ AP propagation, heart contracts Heart relaxes but has less time to

fill with blood Time Arrhythmia RyR, Ryanodine Receptor; SR, sarcoplasmic reticulum; AP, action potential; Ca2+, calcium Sources: Proprietary data from Priori Lab

Rationale for CASQ2 Overexpression

in RYR2 CPVT (cont.) CASQ2 Overexpression Leads to Increased Ca2+ Buffering to Counteract Ca2+ Sensitivity of RYR2 Mutant RyR, Ryanodine Receptor; SR, sarcoplasmic reticulum; AP, action potential; Ca2+, calcium Sources: Proprietary data from Priori

Lab RYR2 Mutation-related CPVT + Overexpressed CASQ2 In addition to stabilizing RYR2 in the closed state, increased CASQ2 enhances Ca2+ buffering, so RYR2 senses less Ca2+ extending diastole until the typical time of contraction, allowing the heart

to fill fully SR Free Ca2+ AP propagation, heart contracts Heart relaxes and fills with blood Time CASQ2 CASQ2 CASQ2 CASQ2 Ca2+ CASQ2 Ca2+ CASQ2 Normal Rhythm Overexpressed CASQ2 increases time to reach threshold for SR Ca2+ release

Elimination of Arrythmias in

Multiple Disease State Models Data Suggests CASQ2 Augmentation Was Well Tolerated & Highly Protective CASQ2 & RYR2 CPVT Arrhythmias ***P<0.001, AAVa-CASQ2-treated vs untreated and AAVa-CASQ2-treated vs

AAVa-GFP-treated 1. Priori Lab, unpublished data. RYR2mut Animals With Sustained VT (%) AAV8-CASQ2 Dose RYR2 Mouse At 12 weeks old, none of the RYR2 mutant mice treated with AAVb-CASQ2 gene therapy exhibited arrhythmias1

Elimination of Arrythmias in

Multiple Disease State Models Data Suggests CASQ2 Augmentation Was Well Tolerated & Highly Protective CASQ2 & RYR2 CPVT Arrhythmias ***P<0.001, AAVa-CASQ2-treated vs untreated and AAVa-CASQ2-treated vs

AAVa-GFP-treated 1. Denegri, et al. 2014 CASQ2 Mouse Significantly fewer CASQ2 mutant mice experienced arrythmias two months after AVVa-CASQ2 gene therapy1 40-50% transduction, achieved in both neonates and adult mice, prevented propagation of

triggered beats1 CASQ2mut Animal with VT (%) 6 9 12 Months After AAVa-CASQ2 Treatment WT Untreated AAVa-CASQ2-treated AAVa-GFP-treated *** *** *** ***

CPVT IND Planned for Q1 2025,

Potentially Followed by Multiple Ex-US CTAs Regulatory interactions intended to shed light on regulators' thinking for addressing multiple genetic mutations (RYR2 & CASQ2) with single gene replacement therapy UK, NL, IT sites planned

in addition to US as part of development Plan to apply for Innovative Licensing & Access Pathway in the UK with aim to accelerate time to market through iterative discussions with MHRA/HTA partners Orphan Drug Designations obtained in EU and US,

seeking rare pediatric disease designation in the US Plan global health authority communications in advance of IND/CTA to de-risk IND enabling nonclinical study execution & clinical study design

BAG3 mutations lead to reduced BAG3

protein leading to dilated cardiomyopathy (DCM) Postulated mechanism: Decreased BAG3 protein leads to heat shock protein dysfunction, and a build-up of dysfunctional proteins in the sarcomere, causing myofilament damage and