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Executive Summary

EDG-7500 is a cardiac sarcomere modulator that slows contraction and enhances relaxation without inhibiting peak myosin contractile force, designed to treat hypertrophic cardiomyopathy while avoiding the heart failure risk associated with cardiac myosin inhibitors.

EDG-7500

Cardiac sarcomeric target · Small molecule

Phase 2 Wholly-owned

Target: Cardiac sarcomeric target

Full NameUndisclosed cardiac sarcomeric target

PathwayCardiac contraction and relaxation

See Target Biology →

Mechanism of Action[Pres '26 S20]✓

TypeCardiac sarcomere modulator

DescriptionEDG-7500 slows contraction and enhances relaxation, without inhibiting peak myosin contractile force, which improves overall diastolic function. This approach is designed to avoid excessive drops in systolic performance that can lead to heart failure risk.

DifferentiationUnlike cardiac myosin inhibitors (CMIs) that carry black box warnings for heart failure, EDG-7500's mechanism is designed to maintain systolic function while improving diastolic function, potentially avoiding the need for REMS requirements and frequent LVEF monitoring.

Indications: Hypertrophic Cardiomyopathy

Target Biology[Pres '26 S20]✓

In hypertrophic cardiomyopathy, the heart muscle becomes abnormally thick and stiff, impairing the heart's ability to relax and fill with blood properly. EDG-7500 modulates the cardiac sarcomere to slow contraction and enhance relaxation, improving overall diastolic function without excessively reducing systolic performance.

Clinical Data

CIRRUS-HCM Part B[Pres '26 S21]✓

Phase 2 Completed n=oHCM patients

Design: Fixed dose study in obstructive HCM

Arms: 50 mg, 100 mg

Endpoints

Endpoint	Result
Primary: Safety and tolerability[Pres '26 S21]✓ Safety assessments	Well tolerated
LVOT gradient response[Pres '26 S21]✓	89% of oHCM patients showed complete LVOT-G response at 100 mg (resting and Valsalva gradients <30 mmHg and <50 mmHg respectively)
NYHA class improvement[Pres '26 S21]✓	78% achieved ≥1 NYHA class improvement at 100 mg vs 43% at 50 mg

Biomarkers

Biomarker	Result	Significance
NT-proBNP[Pres '26 S21]✓	56% achieved NT-proBNP <150 pg/mL at 100mg	NT-proBNP is a marker of heart failure and cardiac stress; reductions indicate improved cardiac function

Safety

Well tolerated with rapid multi-domain improvements

CIRRUS-HCM Part C[Pres '26 S22]✓

Phase 2 Completed n=nHCM patients

Design: Fixed dose study in nonobstructive HCM

Arms: 50 mg, 100 mg

Endpoints

Endpoint	Result
Primary: Safety and tolerability[Pres '26 S22]✓ Safety assessments	Well tolerated
KCCQ-CSS clinical improvement[Pres '26 S22]✓	88% of nHCM participants had KCCQ-CSS clinical improvement with robust absolute improvements

Biomarkers

Biomarker	Result	Significance
NT-proBNP[Pres '26 S22]✓	55% reduction by Week 1	Rapid reduction in cardiac stress marker indicating early therapeutic benefit
e' (diastolic function marker)[Pres '26 S22]✓	Rapid changes as early as one week	e' measures diastolic function; improvements indicate better cardiac relaxation

Safety

Well tolerated

CIRRUS-HCM Part D[Pres '26 S23]✓

Phase 2 Ongoing n=Target 50-60 patients

Design: 12-week goal-directed dose escalation study in both oHCM and nHCM

Arms: oHCM dose escalation, nHCM dose escalation

Endpoints

Endpoint	Result
Primary: Safety[Pres '26 S23]✓ Safety and tolerability assessments	Favorable interim safety results announced
Efficacy assessments[Pres '26 S23]✓	NT-proBNP, Cardiac Troponin I, KCCQ, NYHA and LVOT-G assessments ongoing

Safety

Favorable interim safety results; no LVEF drops <50% observed across all studies

Competitive Landscape

Competitors

Drug	Company	Limitation
mavacamten (CAMZYOS)	Bristol-Myers Squibb	Black box warning for heart failure, REMS requirement, frequent LVEF monitoring, only approved for oHCM
aficamten (MYQORZO)	Cytokinetics	Black box warning for heart failure, REMS requirement

Investment Analysis

Satya Bio Analysis — estimates based on public data and analyst judgment, not sourced from company materials

Bull Case

Thesis Point	Supporting Evidence	Confidence
Differentiated mechanism avoids heart failure risk enabling broader market access	No LVEF drops <50% across studies, efficacy in both oHCM and nHCM, physician enthusiasm for safety profile	Medium
Large addressable market with significant unmet need	~165K symptomatic HCM patients, no approved nHCM therapies, limitations of current CMIs	High

Bear Case

Risk	Evidence	Mitigating Factors
Small Phase 2 studies may not translate to Phase 3 success	Limited patient numbers in proof-of-concept studies, high bar for HCM efficacy	—
Competitive pressure from established CMIs with proven efficacy	mavacamten and aficamten already approved with clinical experience, physician familiarity	—

Key Debates

Question	Bull View	Bear View	Resolution Catalyst
Can EDG-7500 demonstrate differentiated efficacy while maintaining safety advantages?	Novel mechanism provides best-in-class profile with efficacy in both oHCM and nHCM	Mechanism may limit peak efficacy compared to direct myosin inhibition	Phase 3 head-to-head or cross-trial comparisons with established CMIs

Market Opportunity[Pres '26 S26]✓

Total Addressable Market

~$10 Billion total potential HCM market

Patient Population

~165K symptomatic HCM patients in US (~125K oHCM and ~40K nHCM)

Unmet Need: High unmet need due to intrinsic mechanistic limitations of current CMIs including heart failure risk, REMS requirements, and lack of approved therapies for nHCM

Catalysts & Upcoming Events

Event	Timing	Importance	Key Metrics to Watch	Consensus
CIRRUS-HCM Part D Phase 2 results in oHCM & nHCM	H1 2026	critical	Efficacy in dose-optimized study, safety profile, biomarker responses	—
EDG-7500 Phase 3 initiation in oHCM & nHCM	H2 2026	high	Trial design, endpoints, enrollment timelines	—
CIRRUS-HCM Part D 12-week data in oHCM & nHCM	H1 2026	high	KCCQ-CSS improvement, NT-proBNP reduction, LVEF stability, dose optimization results	—
Phase 3 initiation in oHCM & nHCM	H2 2026	high	Trial design, primary endpoints, enrollment strategy, regulatory alignment	—