Pioneering a new class of RNA medicines to increase targeted gene expression May 2025 C O R P O R A T E O V E R V I E W
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CAMP4 overview RAP Platform: regRNAs are master controllers of gene regulation Lead metabolic program: Urea Cycle Disorders Lead CNS program: SYNGAP1-related Disorders 3 Agenda
CAMP4 is the leader in gene regulatory RNA (regRNA) discovery and regRNA-targeting antisense oligonucleotide (ASO) therapies to upregulate gene expression to restore healthy protein levels 4 Our proprietary RAP Platform was built for the discovery of novel regRNAs that regulate the expression of every protein-coding gene Our current focus is on metabolic and CNS genetic diseases where modest increases in protein expression can be clinically meaningful Safety, PK and key biomarker data from Phase 1 study of CMP-CPS-001 for Urea Cycle Disorders expected in Q4 ’25 and advancement of CMP-SYNGAP-01 into GLP tox studies NASDAQ: CAMP There are prevalent diseases where gene upregulation is likely to have a meaningful clinical benefit Pioneering a new class of RNA medicines to increase targeted gene expression
5 World-class management team, experienced board and advisors Josh Mandel-Brehm President & CEO David Bumcrot, PhD Chief Scientific Officer Michelle Gates Chief People Officer Caleb Moore Chief Business Operations Officer Yuri Maricich, MD Chief Medical Officer Kelly Gold Chief Financial Officer Board of Directors James Boylan Ingo Chakravarty Michael Higgins Steven Holtzman Josh Mandel-Brehm Amir Nashat, ScD Paula Ragan, PhD Andy Schwab Murray Stewart, DM FRCP Ravi Thadhani, MD Douglas Williams, PhD Rick Young, PhD Len Zon*, MD *Board observer, co-founder Daniel Tardiff, PhD SVP, Head of Discovery Satya Kuchimanchi, PhD SVP, Technical Operations Alla Sigova, PhD VP, Head of Platform
Program Indication Target Discovery & Preclinical Phase 1 Phase 2 Phase 3 Anticipated Milestones Commercial Rights Metabolic diseases CMP-CPS-001 Urea Cycle Disorders CPS1 Phase 1 MAD data in Q4’25 CMP-CPS-001 Expansion Urea Cycle Disorders- OTC heterozygotes CPS1 CNS diseases CMP-SYNGAP-01 SYNGAP1-related Disorders SYNGAP1 Initiation of GLP tox studies in ‘25 New Named Program Genetically defined Parkinson’s disease (PD) and sporadic PD GBA1 New Discovery Programs CNS & Metabolic Numerous Collaborations Advancing a pipeline in metabolic and CNS genetic diseases 6 Strategic research collaboration leveraging CAMP4’s RAP Platform advancing novel therapeutics that increase protein levels by targeting regRNA sequences for two genetic targets. Active discovery and development of multiple programs utilizing RAP Platform
CAMP4 overview RAP Platform: regRNAs are master controllers of gene regulation Lead metabolic program: Urea Cycle Disorders Lead CNS program: SYNGAP1-related Disorders 7 Agenda
8 regRNAs play a central role in the regulation of every gene’s expression mRNA Activators and repressors bind to regRNAs to control the transcriptional state regRNAs originate from enhancers and promoters to control the expression of protein-coding genes Active Enhancer Nucleus Transcription Factors and Regulators Target Gene Promoter Activators Repressors regRNAActive Enhancer Increased mRNA expression Addresses root cause of haploinsufficient or partial loss-of-function diseases by returning targeted protein levels to within a healthy range ASOs disrupt the interactions between repressors and regRNAs enabling increases in gene expression regRNA (Modulated) Active Enhancer ASO binds regRNA 1 2 3 Source: Sharp et al. (2022) RNA 28: 52-57; Henninger et al. (2021) Cell 184:207-225; Sartorelli & Lauberth (2020) Nat. Struct. Mol. Biol. 27: 521-8; Oksuz et al. (2023) Molecular Cell 83: 2449-63.
9 1. Map candidate regRNAs 2. Generate ASO leads 3. Optimize leads CAMP4’s proprietary RAP Platform catalogs thousands of regRNAs in any tissue and generates ASO leads to increase gene expression Next-gen sequencing and machine learning algorithms map regRNAs controlling every expressed gene. One of the most extensive, proprietary regRNA databases to date across wide range of tissue types. Liver or CNS Rapidly pinpoint regions where ASO binding results in optimal upregulation of a target gene Therapeutic candidates are designed to integrate a range of chemical modifications and tissue-targeting delivery strategies optimizing potency and safety
CAMP4 applies its RAP Platform to genetic diseases where modest increases in gene expression can be clinically meaningful 10 Clinical, Regulatory and CMC • Defined patient population • Efficacy can be evaluated in Ph 1/2 based on availability of biomarkers • Established manufacturing & supply chain • Clear or established path to approval Platform Fit Upregulating target gene by modest amount can provide clinically meaningful benefit Translation and Druggability • Ability to achieve delivery and target engagement in the desired cell type • Compelling preclinical datasets in relevant disease models Increase target gene Increase function Commercial Potential • High unmet need, often life threatening • Differentiated from competition, with attractive revenue potential D is ea se S ev er ity D is ea se S ev er ity Functional benefit is proportional to increased gene expression Functional benefit is a multiple of increased gene expression Potential range of clinically meaningful threshold Severe Healthy Mild Haploinsufficiency 50% activity Potential range of clinically meaningful threshold Severe Healthy Mild Partial loss of function <50% activityPr ot ei n ex pr es si on le ve ls Pr ot ei n ex pr es si on le ve ls
CAMP4 overview RAP Platform: regRNAs are master controllers of gene regulation Lead metabolic program: Urea Cycle Disorders Lead CNS program: SYNGAP1-related Disorders 11 Agenda
Urea Cycle Disorders (UCDs) are a set of life-threatening inherited metabolic diseases characterized by the accumulation of toxic ammonia 12 OTC ASS1 ASL ARG1 CPS1 Dysfunctional Urea Cycle NAGS^ OTC mutated retaining only partial activity UREA AMMONIA Mutation in one of several urea cycle enzymes or transporters causes suboptimal ureagenesis (conversion of ammonia to urea) • Ammonia accumulates to dangerous levels without warning, posing a constant risk of life-threatening hyperammonemic crises and irreversible brain damage • Collectively, we believe there are ~4,300 diagnosed symptomatic patients in the US; potential for opportunity to expand with increased diagnosis rates • CAMP4 UCD severe* opportunity is estimated to be 2,300 diagnosed symptomatic patients out of 3,700 prevalent • Female OTC Heterozygotes represent an estimated incremental 2,000 diagnosed symptomatic patients UCD background • No mutation agnostic disease modifying treatments available • Symptomatic therapies include nitrogen scavengers (3-4 pills / day) and a strict diet that borders on malnutrition • Constant risk of hyperammonemic crises which can be caused by infection, lapse in diet or medications Current standard of care is symptomatic *Enzyme levels >5% of normal, severe symptoms persist beyond the first month of life ^NAGS enzyme produces the co-factor NAG which activates CPS1 Sources: Yilmaz et al. (2022), Buerger et al. (2020), Posset et al. (2019), Sen et al. (2024), Batshaw et al. (1986), Trinity Primary Research – N=6 OTCd KOLs, April 2025, Komodo Claims Data 2016-2024 Trinity Life Sciences analysis of Komodo Claims data shows ~3.1K unique female OTC patients with at least 2 instances of ICD-10 code E72.4 diagnosis from 2016-2024
CMP-CPS-001 is a GalNAc-conjugated ASO that binds to a CPS1-specific regRNA to increase CPS1 expression and upregulate the expression of multiple urea cycle enzymes to amplify the conversion of ammonia to urea, potentially addressing more than 90% of patients with late onset UCDs. 13 CAMP4 is targeting increased expression of CPS1, resulting in amplified ureagenesis and improved conversion of ammonia to urea CPS1 is the gatekeeper of the urea cycle OTC ASS1 ASL ARG1 CPS1 UREA Functional Urea Cycle AMMONIA NAGS^ CMP-CPS-001
14 Clinical observations and prior studies have shown that modest increases in ureagenesis can significantly reduce disease severity Early onset (Mortality at birth) Severe UCDs (~90% patients) OTC female heterozygotes (Range of symptoms) WT Late onset patients (>1 month) CMP-CPS-001 target therapeutic benefit U re ag en es is SeverityFatal Healthy Sources: OTC deficiency prevalence sourced from CAMP4; Diagnosis rate informed by CAMP4 diagnosis rate assumption and extrapolations; ”Gyato et al. (2004) Ann. Neurol. 55(1):80-6, McCullough et al. (2000) Am. J. Med. Genet. 93(4):313-9, Scharre et al. (2022) Ann. Clin. Transl. Neurol. 9(11):1715-26, Sen et al. (2024) Mol. Genet. Genomic Med. 12(4):e2443, Sprouse et al. (2014) Mol. Genet. Metab. 113(1-2):136-41.
CMP-CPS-001 has the potential to be the 1st disease modifying therapy 15 Increase ureagenesis via GalNAc-conjugated ASO *CMP-CPS-001 has been granted Rare Pediatric Disease Designation and Orphan Drug Designation 1x monthly (titratable), subcutaneous • ~90% of severe UCD patients (pediatric and adult) • Female OTC heterozygotes Prevent hyperammonemic crises Reduce or remove scavengers Liberalize protein-restricted diet Nitrogen-binding agent, “scavenger” 1-3x daily, oral liquid Broadly applicable Hyperammonemic crises risk Significant pill burden Strict protein-restricted diet CMP-CPS-001* Anticipated Profile Standard-of-Care (symptomatic) D es cr ip tio n Po pu la tio n
16 CMP-CPS-001 targets the key regRNA controlling CPS1 expression RAP Platform identified CPS1 regRNA CMP-CPS-001 increases CPS1 mRNA in primary WT liver cells CPS1 promoter CPS1 enhancers: Target of CMP-CPS-001 CPS1 gene Activity confirmed in OTC deficient donor cells with CMP-CPS-001 analog (clinical candidate without GalNac) NTC = non-targeting control CPS1 regRNA regRNA Clinical candidate: CMP-CPS-001 First- pass Screen Tiling Fine- tuning Donor 1 Donor 2
ASO targeting mouse Cps1 regRNA in Otc-deficient mice reduces ammonia and supports once-monthly dosing 17 Onset Maintenance Return (1-2 wks) (~4 wks) (~1-2 wks) • The Otcspf-ash mouse model carries a patient mutation in Otc that reduces mRNA levels • Otc activity is 5%-10% of wild-type1 • Model displays elevated ammonia relative to wild- type mice following an acute ammonia challenge • ASO was shown to cause significant ~50% reduction in toxic ammonia (approx. WT levels) • Correlated with ~20% increase in urea production (data no shown) • Maximal effect achieved in 2-3 weeks • Response persisted for ~1 month 1Hodges and Rosenberg, PNAS, 1989
18 Using 13C-Sodium Acetate for ureagenesis in WT NHP NHP administered drug once-monthly. Ureagenesis assessed up to 30 days after final dose. Data shown is one week after a second dose. Error bars represent standard error of the mean; PBS denotes phosphate-buffered saline; * denotes p<.05; ** denotes p<.01. ~↑40% Using ureagenesis rate test (URT), CMP-CPS-001 was shown to increase ureagenesis up to 40% in wildtype cynomolgus monkeys 0 60 120 180 240 0 500 1000 1500 2000 2500 min (t) U re ag en es is A UC (μ M x m in ) Ureagenesis AUC (13C-Urea) * **5 mg/kg CMP-CPS-001 PBS URT uses 13C-labeled sodium acetate to measure ureagenesis CMP-CPS-001 increases ureagenesis in NHPs
19 Clinical Program Update: CMP-CPS-001 expansion into Ph 1b in OTC heterozygotes MAD* HV - data expected in Q4 2025 Cohort 2 Cohort 3 Cohort 4 Dosing complete PRIMARY FOCUS: safety, inform MAD PRIMARY FOCUS: safety and pharmacokinetics / pharmacodynamics (URT) Cohort 1 (4 mg / kg) (1.8 mg / kg) (0.6 mg / kg) (0.2 mg / kg) Cohort 1 Cohort 2 Dosing complete *SAD and MAD utilize same dose scheme PRIMARY FOCUS: safety, pharmacokinetics / pharmacodynamics (URT) in OTC heterozygotes Anticipated OTC expansion SAD* HV - completed Cohort 3 Cohort 4 OTC heterozygote cohort *n=10- 12 participants per cohort, 3:1 randomization drug to placebo. MAD frequency is q28 days x 3 doses. Subcutaneous administration.
20 Phase 1 SAD safety and PK summary (all cohorts 1 – 4) SAD portion of study completed. Conducted planned interim analysis of safety data for 48 normal healthy volunteer participants. 4 Cohorts of 12 participants each, randomized 3:1 investigational product to placebo; 36 individuals received a single subcutaneous dose of CMP-CPS-001. CMP-CPS-001 was well tolerated, with no evidence of a maximum tolerated dose. No safety trends of concern have been observed, including no treatment-emergent serious adverse events. Pharmacokinetic data similarly was observed to be consistent with expectations, demonstrating a dose- dependent increase in exposure with clear separation between dose levels. Safety results were favorable and consistent with profiles of approved liver- targeted ASOs, with all TEAEs being Grade 1 (mild) or Grade 2 (moderate) with no concerning safety trends.
21 Ongoing trial has the potential to support a combined Phase 2/3 study Safety Pharmacokinetics Ureagenesis rate test (PD) • Vitals • Cardiac monitoring • Liver function tests • Immunogenicity • Plasma and urine measurements • Compare human pharmacokinetic behavior to pre-clinical data observations • Observe that human PK achieves levels expected to demonstrate efficacy on ammonia and ureagenesis in animal studies • Ureagenesis measures rates of flux through the urea cycle • Rates of ureagenesis correlate with reduction in ammonia (approvable endpoint) • URT utilized by other programs to correspond with clinically meaningful dropping of low protein diet and scavenger (supportive care measures) Key Endpoint(s) in one or more anticipated Phase 2 / 3 Trials: • Ammonia (recognized approvable endpoint) • Diet liberalization (Responder analysis) • Nitrogen Scavenger reduction (Responder Analysis) 1 2 3 Data Elements • Ureagenesis, Plasma glutamine • Clinical events
CAMP4 overview RAP Platform: regRNAs are master controllers of gene regulation Lead metabolic program: Urea Cycle Disorders Lead CNS program: SYNGAP1-related Disorders 22 Agenda
SYNGAP1 is a haploinsufficiency with 10,000+ US patients in need of therapy 23 Haploinsufficiency results in 50% of normal protein levels 10,000+ SYNGAP1 patients in the US High unmet need for disease-modifying therapy 6.1–10 per 100K incidence rate 1,2 ~85% have seizures, potentially experiencing 10+ per day 3,4,5 ICD-10 code assigned in 2021 0 approved therapies SYNGAP1 Haploinsufficiency 50% SynGAP protein 1 López-Rivera et al., Brain, 2020; 2 Marotta et al., Curr Probl Pediatr Adolesc Health Care, 2024; 3 Holder et al., GeneReviews, 2019; 4 SYNGAP1-Related Epilepsy, Epilepsy Foundation (Accessed May 2025); 5 Vlaskamp et al. Neurology, 2019 SYNGAP1 SYNGAP1
Dire unmet need for a targeted disease modifying therapy to alter SYNGAP1 disease course 24 Complex Symptoms No Approved Therapy Non-specific treatments have limited impact on SYNGAP1 symptoms − Anti-seizure medications − Cannabinoids − Sleep medications Polypharmacy is common – Patient regimen 6 example: − Epidiolex − Ravicti − Sodium bicarb − Amantadine Constant patient care needed and caregiver worry − Trazodone in PM − Melatonin in PM − 1:1 CBD/THC in PM − Small dose of Onfi Sleep problems ~60% of patients 2,5 Developmental delay and/or intellectual disability 100% of patients 1,2,3 Generalized epilepsy ~85% of patients 3,4,5 Severe behavioral problems ~70% of patients 1,5 Limited communication ~30% non-verbal, single words 4 1 Wiltrout, et al., Epilepsia, 2024; 2 Jimenez-Gomez, et al. J Neurodev Disord, 2019; 3 Holder et al., GeneReviews, 2019; 4 SYNGAP1-Related Epilepsy, Epilepsy Foundation (Accessed May 2025); 5 Vlaskamp et al. Neurology, 2019; 6 SynGAP Research Fund (SRF)
CAMP4 aims to increase SynGAP protein levels to restore SynGAP at the synapse and improve disease symptoms 25 Mutations in SYNGAP1 lead to decreased SynGAP protein, causing increased synaptic firing Neuronal Excitability 1 Illustrative depiction of Electroencephalogram EEG1 Reduced SynGAP-PSD95 complexes; increased post-synaptic AMPAR at baseline 50% SynGAP protein PSD95 SynGAP AMPAR Glutamate Presynapse Postsynapse EEG1 Restored SynGAP-PSD95 complexes; restored post-synaptic AMPAR at baseline Increased SynGAP protein PSD95 SynGAP AMPAR Glutamate Presynapse Postsynapse CMP-SYNGAP-01 CMP-SYNGAP-01 binds to a SYNGAP1-specific regRNA to increase SYNGAP1 expression, aiming to restore SynGAP towards wild-type levels and normalize synaptic function Restored Neuronal Excitability
Targeting SYNGAP1 regRNA increases transcriptional machinery and nascent transcription 26 ASO binding to SYNGAP1 regRNA increases RNA Pol II recruitment at SYNGAP1 promoter RegRNA-targeting ASO increases nascent RNA A B C SYNGAP1 promoter regions Human SYNGAP1 regulatory regions • Increased RNA Polymerase II at SYNGAP1 promoter (Chromatin Immunoprecipitation) • All groups treated with regRNA-targeting ASO • Data normalized to NTC for both control genes and SYNGAP1 • Increased SYNGAP1 nascent transcription • Nascent transcription analysis of cells treated with NTC or ASO • Data normalized to NTC NTC CMP-SYNGAP-01 NTC CMP-SYNGAP-01 0.0 0.5 1.0 1.5 2.0 2.5 Fo ld C ha ng e N or m al iz ed to N TC Nascent SYNGAP1 mRNATotal SYNGAP1 mRNA
27 Targeting SYNGAP1 regRNA restores wild-type SYNGAP1 levels in patient iPSC-derived neurons compared to familial control NTC = non-targeting control Patient with a heterozygous nonsense mutation in Syngap1 (K1185X) and their healthy familial control 6. 25 12 .5 25 50 10 0 20 0 6. 25 12 .5 25 50 10 0 20 0 6. 25 12 .5 25 50 10 0 20 0 0.0 0.5 1.0 1.5 2.0 FC in S YN G AP 1 m R NA N or m al iz ed to H ea lth y Fa m ili al C on tr ol Familial Control SYNGAP Patient NTC- ASO NTC- ASOCMP-SYNGAP-01 50% ↓ in patient neurons 100% ↑ in patient neurons with ASO SY N G A P1 m R N A Fo ld C ha ng e N or m al iz ed to Fa m ili al C on tr ol NTC- ASO CMP-SYNGAP-01
28 CMP-SYNGAP-01 restores near-normal protein levels in Humanized Mouse Model Haploinsufficient for SynGAP Haploinsufficient Mouse • No copies of mouse Syngap1 • Single copy of Human SYNGAP1 Homozygous Mouse • No copies of mouse Syngap1 • Two copies of Human SYNGAP1 D1 D15 ICV Terminal Protein Mouse age: P21 aCSF = artificial CSF ****, p<0.0001 (SYNGAP1-ZBTB9)1Bpro/Mmjax mouse strain obtained from the Mutant Mouse Resource and Research Centers (originally deposited by Benjamin Prosser, Ph.D., University of Pennsylvania). - aCSF 25ug 50ug 100ug 0.00 0.25 0.50 0.75 1.00 1.25 FC in S yn G A P Pr ot ei n N or m al iz ed to H om oz yg ou s C on tr ol Haploinsufficient Homozygous Control ✱✱✱✱ ns ns ✱✱✱ Sy nG A P Pr ot ei n Fo ld C ha ng e N or m al iz ed to H om oz yg ou s C on tr ol
CMP-SYNGAP-01 rescues motor function deficits and increased activity of Humanized Mouse Model Haploinsufficient for SynGAP 29 Hyperactivity & anxietyMotor function Increased activity is rescued (PalmReader) Motor defects are rescued (Rotarod) Spatial learning defect is rescued (Y-Maze) Cognition & memory *, p <0.05 **, p<0.01 aCSF = artificial CSF ***, p<0.001 SynGAP protein levels are increased ASO treatment increases SynGAP protein levels by 1.5- 1.7-fold P27 Rotarod Takedown Y-MazePalmReader 2 x ICV injections (30 ug / dose) • Hom- aCSF (N=12) • Haplo- aCSF (N=18) • Haplo- ASO (N=10) P2 P15-23P5
30 Nonhuman Primate PK/PD Study to Assess CMP-SYNGAP-01 Pharmacology aC SF Q2w x3 low Q2w x3 mid Q2w x3 high Q2w x3 C M P- SY N G AP -0 1 TA Dose Dosing frequency Cynomolgus monkey Study Design Key Takeaways • CMP-SYNGAP-01 was clinically well-tolerated at all dose levels • IT administration achieved dose-linear exposure across brain regions • Deeper brain structures (e.g., substantia nigra, caudate, etc.) had lower ASO concentrations • SynGAP protein increased ~1.5-fold across brain regions implicated in disease• Intrathecal administration • N = 4 animals/group • Formulated in aCSF D1 D43 IT D15 D29 IT IT Terminal Protein mRNA ASO 24 hr PK24 hr PK 24 hr PK CSF CSF CSF CSF
Dose-linear increases of CMP-SYNGAP-01 levels across brain regions following repeat IT administration 31 Highest ASO levels observed in brain regions primarily involved in SYNGAP1-related disorders • Dose-linear CMP-SYNGAP-01 concentrations achieved with repeat IT administration • Generally, even distribution across multiple disease-relevant brain regions • Lower ASO levels observed in deep brain regions, consistent with known ASO biodistribution following IT administration aCSF = artificial CSF C M P- SY N G AP -0 1 (µ g/ g)
Intrathecal administration of CMP-SYNGAP-01 to monkeys resulted in a ~50% increase in SynGAP protein 32 0 1 2 3 Fo ld c ha ng e N or m al iz ed to a C SF ns ✱ ✱✱✱✱ 0 1 2 3 Fo ld c ha ng e N or m al iz ed to a C SF ns ✱✱✱ ✱✱ 0.0 0.5 1.0 1.5 2.0 2.5 Fo ld c ha ng e N or m al iz ed to a C SF ✱ ns ✱ 0 1 2 3 Fo ld c ha ng e N or m al iz ed to a C SF ns ns ns Frontal Cortex Occipital CortexHippocampus Motor Cortex Intellectual Disability Learning & Memory EEG signature Motor function aCSF low mid high aCSF = artificial CSF *, p <0.05 **, p<0.01 ***, p<0.001 ****, p<0.0001 Sy nG AP P ro te in N or m al iz ed to a C SF Sy nG AP P ro te in N or m al iz ed to a C SF Sy nG AP P ro te in N or m al iz ed to a C SF Sy nG AP P ro te in N or m al iz ed to a C SF
33 CAMP4 positioned to be first in the clinic for SYNGAP> 1 yr, 100 pts of data obtainable from natural history study Standard-of-Care Natural History Study No disease modifying therapies available Patients currently treated using a polypharmacy approach of symptomatic treatments Third party SRF sponsored study is ongoing, advocacy / center of excellence driven > 1 yr, 100 pts of data obtainable from natural history study Existing center of excellence is central node for translational / clinical excellence Center-of-Excellence GLP toxicity studies expected to initiate in 2025 Potential for CMP-SYNGAP-01 to be first clinical candidate evaluated in patients Path to Approval Established path to approval for a developmental epileptic encephalopathy (DEE) Seizure quantification as primary + neurodev. scale Path to Clinic
CAMP4 is the leader in gene regulatory RNA (regRNA) discovery and regRNA-targeting antisense oligonucleotide (ASO) therapies to upregulate gene expression to restore healthy protein levels 34 Our proprietary RAP Platform was built for the discovery of novel regRNAs that regulate the expression of every protein-coding gene Our current focus is on metabolic and CNS genetic diseases where modest increases in protein expression can be clinically meaningful Safety, PK and key biomarker data from Phase 1 study of CMP-CPS-001 for Urea Cycle Disorders expected in Q4 ’25 and advancement of CMP-SYNGAP-01 into GLP tox studies NASDAQ: CAMP There are prevalent diseases where gene upregulation is likely to have a meaningful clinical benefit Pioneering a new class of RNA medicines to increase targeted gene expression
Thank you May 2025 C O R P O R A T E O V E R V I E W