Pre-IND · PAR4 Antagonist · Vanderbilt Spinout · $10M Seed

First-in-Class Drug &
Diagnostic for
Perimenopausal Thromboinflammatory
Cardiovascular Disease

SEP-001 PAR4 antagonist and ThromboRisk™ companion diagnostic — targeting the only unaddressed axis of cardiovascular risk in women during and after the perimenopausal transition.

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SEP-001 · PAR4 Antagonist ThromboRisk™ Panel Vanderbilt Drug Discovery May 2026 · Confidential
0
Approved Therapies Targeting PAR4 Thromboinflammation
The 2020 AHA Scientific Statement on menopause and CVD (El Khoudary et al., Circulation 2020;142:e506) reviewed every known cardiovascular risk axis. The PAR4-driven thromboinflammatory pathway is absent. Septagen is building the first therapy to address it.
50M+
US Women in Perimenopause & After
No existing therapy addresses the thromboinflammatory axis in this population. Zero.
2×
CV Mortality Increase
Risk begins inflecting during perimenopause — not after the transition ends. The thromboinflammatory cascade activates as estrogen declines, not after it disappears.
3×
PAR4 PMP Drive vs PAR1
PAR4 generates 3× more platelet microparticles than PAR1 — the unaddressed thromboinflammatory driver (Hamm lab, PMID 23307185).
<5%
HRT Penetration in High-Risk Populations
Even optimal HRT cannot address PAR4-driven epigenetic changes in bone marrow megakaryocytes.
The Opportunity

Women's Cardiovascular Risk Doesn't Accumulate — It Inflects

The perimenopausal transition is a coordinated biological event and the critical intervention window. As estrogen declines — not just after it disappears — F2RL3 demethylation activates the thromboinflammatory cascade. Waiting until a woman is fully postmenopausal means the PAR4 overdrive has already been running for years.

In 2020, the American Heart Association published its first-ever Scientific Statement on menopause transition and cardiovascular disease risk (El Khoudary et al., Circulation 2020;142:e506–e532) — the field's definitive reference. It formally recognised perimenopause as the period of greatest cardiovascular risk acceleration, and comprehensively reviewed lipids, blood pressure, vascular remodeling, adiposity, and metabolic risk. The PAR4-driven thromboinflammatory axis is absent. No approved therapy addresses it.

HRT initiated early attenuates cardiovascular risk (KEEPS, ELITE, WHI re-analyses). The problem: HRT penetration remains below 5% even in high-risk populations. And even optimal, well-timed HRT does not address the thromboinflammatory axis.

Women's heart disease is microvascular: clear arteries, microclots, and inflammation — not plaque occlusion. Existing therapies are built for the wrong model.

Key Insight
"A woman in perimenopause — still cycling, not yet technically menopausal — can already carry elevated PAR4-AI, elevated PMP burden, and advancing thromboinflammatory disease. The window to intervene is earlier than the field has recognised."
CV Disease Risk Elevation Post-Menopause
% increase vs. premenopausal baseline · conditions driven by PAR4/thromboinflammatory axis highlighted
PAR4 / Thromboinflammatory axis — addressed by SEP-001
Broader cardiovascular axis
Sources: AHA Circulation 2020; European Heart Journal 2022 (n=1.4M women); Go Red for Women / NHANES
The Treatment Landscape

Three Axes of Menopause CV Risk — One Unaddressed

Treatment Axis HRT NK3 Antagonists (Veozah · Lynkuet) SEP-001 (PAR4) HRT + SEP-001
CNS Symptom Relief
Hot flashes · sleep · mood · cognition
 YesYesNoYes
Peripheral Endothelial / Lipid
Vascular tone · LDL · eNOS — early window only
 PartialNoNoPartial
Peripheral Thromboinflammatory
PAR4 · microclots · PMP burden · NETosis
 NoNoYES ◆YES ◆
The thromboinflammatory axis is the only axis where NO existing therapy — hormonal or non-hormonal — provides coverage. SEP-001 addresses it directly. Every fezolinetant (Veozah) and elinzanetant (Lynkuet) prescription creates a symptom-controlled patient with zero thromboinflammatory protection.
CNS Symptom Relief
Hot flashes · sleep · mood · cognition
HRT
Yes
NK3 Antagonists (Veozah · Lynkuet)
Yes
SEP-001 (PAR4)
No
HRT + SEP-001
Yes
Peripheral Endothelial / Lipid
Vascular tone · LDL · eNOS — early window only
HRT
Partial
NK3 Antagonists (Veozah · Lynkuet)
No
SEP-001 (PAR4)
No
HRT + SEP-001
Partial
⬥ Peripheral Thromboinflammatory
PAR4 · microclots · PMP burden · NETosis
HRT
No
NK3 Antagonists (Veozah · Lynkuet)
No
SEP-001 (PAR4)
YES ◆
HRT + SEP-001
YES ◆
The thromboinflammatory axis is the only axis where NO existing therapy — hormonal or non-hormonal — provides coverage. SEP-001 addresses it directly.
The Mechanism

PAR4: A Targetable, Biomarker-Identifiable
Driver of Thromboinflammation

01
Estrogen Decline (Perimenopause)
The thromboinflammatory cascade activates as estrogen declines — during perimenopause — not only after it disappears. F2RL3 methylation changes begin in megakaryocyte progenitors, endothelial cells, and immune cells as estrogen levels fluctuate and fall during the perimenopausal transition.
02
PAR4 Overexpression
PAR4 overexpression and F2RL3 hypomethylation — persistent and incompletely reversed by HRT. F2RL3 hypomethylation predicts CV mortality (ESTHER cohort, PMID 24510982). PAR4 is upregulated across multiple estrogen-responsive cell types.
03
PAR4 Upregulation
Increased PAR4 expression on platelets; elevated thrombin sensitivity; loss of estrogen-mediated platelet quiescence. Cathepsin G provides a third PAR4 activation axis.
04
PMP Storm
PAR4 drives 3× more platelet microparticle release than PAR1 via Rho-kinase/MLC axis. PMPs carry 5–100× the procoagulant activity of resting platelets (PMID 23307185).
05
Thromboinflammatory Loop
PMPs deliver P-selectin, CXCL4, CCL5 to vascular and immune cells — a self-amplifying loop that vorapaxar (PAR1 antagonism) leaves entirely intact.
3×
PAR4 PMP Drive vs PAR1
PAR4 generates 3× more platelet microparticles via Rho-kinase/MLC axis. PMPs carry 5–100× the procoagulant activity of resting platelets. This is the mechanism vorapaxar does not address.
F2RL3
PAR4 Overexpression
PAR4 overexpression and F2RL3 hypomethylation across estrogen-responsive cell types creates persistent thromboinflammatory risk — independent of circulating estrogen and incompletely reversed by HRT.
Vorapaxar Gap
Why PAR1 Antagonism Is Not Enough
Vorapaxar showed reduced MACE but carries bleeding liability and leaves PAR4-driven microparticle thromboinflammation intact. SEP-001 preserves PAR1-mediated hemostasis while targeting the residual PAR4 axis.
BMS Validated IP Gap
Class Safety Proven · Septagen Owns the Women's Health IP
BMS advanced PAR4 to Phase 2 — no bleeding signal. BMS externalized the program. BMS's broad PAR4 IP explicitly excludes women's health indications. Septagen filed compound + indication. We occupy the exact space BMS cannot reach.
The Therapeutic

SEP-001: Potent, Selective PAR4 Antagonist
from World-Leading Discovery Program

Vanderbilt Drug Discovery has advanced 12+ drugs to the clinic. SEP-001's benzofuran-thiadiazole scaffold is differentiated from BMS's discontinued program. Lindsley's lab is actively progressing a series of follow-on PAR4 antagonist compounds.

12+
Drugs advanced to clinic by Vanderbilt Drug Discovery
AKI
First in vivo efficacy in ischemia-reperfusion model
Pre-IND
IND-enabling studies defined and in progress
No Bleed ✓
No increase in bleeding at pharmacologically active doses
Development Progress
✓
Lead ID
✓
In Vivo
✓
PK
→
IND-Enabling
○
IND Submit
Key Pharmacokinetic Properties
~30h
Plasma Half-Life
QD
Once-Daily Dosing
High
Oral Tissue Distribution
Oral
Chronic Prevention
In Vivo Efficacy — AKI Dose-Dependent Survival
Vehicle (control)
SEP-001 1mg/kg
SEP-001 5mg/kg
p = 0.0028 (Chi-Square) · Resembles PAR4 knockout phenotype
The Diagnostic

ThromboRisk™ Panel: Revenue-Generating Companion Diagnostic

1
Genomic
F2RL3 CpG Methylation Status
CPT 81479 · 81599 · Thr120Ala PAR4 SNP
Baseline molecular risk. PAR4 overexpression and F2RL3 hypomethylation are associated with elevated cardiovascular risk — including gain-of-function SNP in women of African descent. Establishes risk independent of HRT status.
2
Functional
PAR4 Activation Index (PAR4-AI)
CPT 85576 · Flow cytometry · AYPGKF agonist
Real-time platelet activation state. Quantifies current thromboinflammatory activity via P-selectin surface expression by flow cytometry. Confirms pharmacological target engagement and enables precision dosing.
3
Burden
CD41+/PS+ PMP Burden · hsCRP · IL-6
LDT · AMA PLA pathway
Downstream disease burden. Direct measure of PAR4-driven thromboinflammation. Monitors treatment response and residual risk over time.
Why ThromboRisk™ is a Moat, Not a Feature
$7M
Pathway to commercial CLIA lab launch
2 yrs
Timeline to revenue generation
40–50%
Acquisition premium — CDx assets command vs. drug-only at M&A
AMA PLA
Dedicated CPT code — next milestone
  • Companion diagnostic IP filed alongside SEP-001 — bundled asset raises acquiror switching costs and supports a 40–50% acquisition premium.
  • PAR4 overexpression and F2RL3 hypomethylation as a biomarker axis represents a novel and unpublished pharmacoepigenomic approach — first-mover advantage in precision platelet biology.
  • PAR4-AI provides a validated pharmacodynamic readout of PAR4 target engagement — enabling precision dosing and label differentiation in a patient population where no approved therapy has previously measured this axis.
  • Three-tier architecture supports independent reimbursement at each stage: screening, treatment gating, and monitoring.
  • Hamm lab postmenopausal donor platelet bank provides proprietary translational data unavailable to competitors.
Platform Architecture

A Three-Ring Platform Built Around the PAR4 Axis

The same compound. The same mechanism. Three concentric rings of clinical and commercial value — each unlocked by the same IND, the same biomarker, and the same ThromboRisk™ Panel.

LEAD
SEP-001 · PAR4 Antagonist
Perimenopausal & Menopausal CV Prevention
  • Primary indication · seed-funded deliverable · outlicense anchor
  • Stage: Pre-IND · Vanderbilt spinout
  • Catalyst: IND + FIH submission → immediate outlicense
  • Paired with ThromboRisk™ CDx for biomarker-selected prescribing
NEAR-TERM
SEP-001 · Indication Expansion
Same Compound · No New IND Required
  • Acute Kidney Injury (AKI): in vivo efficacy confirmed in IRI model (Erreger et al. 2023); mechanistic follow-up manuscript submitted to Journal of the American Society of Nephrology (bioRxiv 2026.03.27.714572)
  • Surgical menopause / POI: abrupt estrogen withdrawal, highest PAR4 activation
  • Aromatase inhibitor users: iatrogenic estrogen deficiency in ER+ breast cancer survivors
PLATFORM
PAR4 Franchise
Long-Range · Partner-Funded
  • Cancer-associated thrombosis: PAR4 upregulated in 32 TCGA tumour types
  • Sickle cell disease: PAR4-driven vaso-occlusive crisis
  • Next-gen analog series in development — Lindsley lab
  • Partner funds platform. Septagen does not carry Phase 1.
One transaction, three rings of value. The acquiror inherits the Lead indication, the Near-Term expansion pipeline, and the Platform franchise in a single deal — with the ThromboRisk™ Panel as the precision patient selection tool across all three.
Target Populations

Four High-Value Target Populations

No franchise currently targets estrogen-deficiency–driven thromboinflammation. Septagen occupies that gap and complements existing portfolios rather than displacing them.

50M+
Perimenopausal & Menopausal Women
Age 45–65 · Thromboinflammatory risk begins during the transition
  • Residual CV risk despite statin / aspirin therapy
  • Elevated hsCRP and inflammatory markers
  • HRT refusal or contraindication — PAR4 is hormone-free
~500K
Surgical Menopause / POI
Abrupt estrogen withdrawal at any age
  • Earlier and more severe thromboinflammatory activation
  • Higher cumulative lifetime CV risk vs. natural menopause
  • HRT often contraindicated (thrombophilia, BRCA, VTE)
3M+
Aromatase Inhibitor Users
ER+ breast cancer survivors
  • Iatrogenic estrogen deficiency — profound and sustained
  • Known CV and thrombotic complications from AI therapy
  • Oncologists seeking cardioprotective adjunct
Growing
NK3 Antagonist Users
Fezolinetant (Veozah) · Elinzanetant
  • Symptom-controlled with zero CV protection
  • Fezolinetant FDA approved May 2023 — market accelerating
  • Every prescription is a patient SEP-001 can serve
The NK3 Tailwind: Every fezolinetant and elinzanetant prescription creates a growing population of symptom-controlled women with zero thromboinflammatory protection. Septagen is the only company positioned to serve them.
Development Strategy

Dual-Asset Strategy: Diagnostic Revenue Funds Drug Development

Current Raise · 18 Months$10M Seed · IND + FIH Sprint
Month 18 · Outlicense TriggerIND Submitted · Partner Takes Over
Partner-Executed · No Septagen CapitalPhase 1 & Beyond
Diagnostic Track
  • Launch ThromboRisk™ LDT diagnostic
  • CLIA validation — all four assay tiers
  • BioVU F2RL3 methylation validation study
  • Apply for AMA PLA dedicated CPT code
  • ThromboRisk™ LDT live — revenue generating
  • CDx package outlicensed alongside SEP-001
  • Diagnostic revenue stream fully established
  • Partner commercialises ThromboRisk™ CDx
  • Recurring revenue: initial screen + 6-month monitoring
  • PMA pathway for FDA-approved CDx indication
Therapeutic Track
  • Lead optimization & SEP-001 compound advancement
  • BioVU epigenomic study (F2RL3 methylation, 50K samples) + prospective human platelet cohort
  • GLP toxicology · hERG · safety pharmacology
  • IND-enabling package · pre-IND FDA meeting
  • Vanderbilt option-to-license executed
  • IND submitted · FIH protocol filed
  • Both assets outlicensed immediately
  • Septagen does not execute Phase 1
  • Partner funds and executes Phase 1
  • Phase 2a: FMD primary endpoint · ThromboRisk™ patient selection
  • Partner executes all subsequent development
Month 18 Milestone
IND submitted · Both assets outlicensed · Partner executes Phase 1
Diagnostic Revenue
ThromboRisk™ LDT live within 18 months · recurring screen + monitoring revenue
Target Exit
$200–$300M upfront · post-IND submission · CDx premium 30–50%
The Team

World-Class Team Built Around the Science

Malcolm Bohm
Malcolm Bohm
MD, PhD · University College London
Co-Founder & CEO
Serial biopharma entrepreneur — Aspreva Pharmaceuticals, Trialytics (acquired by IMS Health), Liquid Grids (acquired by FemTec Health). Senior leadership at Novartis and Pfizer. 25+ years drug development and commercialization.
Heidi E. Hamm
Heidi E. Hamm
PhD · Vanderbilt University
Co-Founder & Chief Scientific Officer
Discovered the PAR4 thromboinflammation pathway. Endowed Chair of Cardiovascular Research, Vanderbilt University. Member, National Academy of Sciences. 360+ publications. Originating scientist behind SEP-001 and the ThromboRisk™ Panel.
Key Advisors
CL
Craig Lindsley, PhD
Medicinal Chemistry
Executive Director, Vanderbilt Drug Discovery. Advanced 12+ clinical candidates. Synthesized SEP-001 and is progressing a follow-on PAR4 antagonist series.
MO
Martin Ogletree, PhD
Scientific Advisor & Board Member
Drug development strategy, indication prioritisation, acquiror landscape navigation, and multi-axis mechanism validation. Extensive cardiovascular and antithrombotic drug development experience.
BB
Brittany Barreto, PhD
Women's Health Strategy
Global authority in femtech and women's health innovation. Former VC. Exited women's health founder. Guides commercial positioning and investor narrative.
DG
Dave Gailani, MD
Medical Advisory Board · Coagulation
Coagulation biology and hemostasis, Wake Forest University School of Medicine. Expert in contact pathway activation, thrombin generation, and the platelet–coagulation interface — directly relevant to PAR4 mechanism characterization and IND-enabling safety package.
AK
Amrita Karve, MD
Medical Advisory Board · Cardiology
Interventional cardiologist, Phoenix. Women's cardiovascular disease, coronary artery disease, and CV risk stratification. Clinical perspective on ThromboRisk™ Panel prescriber adoption and SEP-001 commercial positioning.
EW
Emma Webb
Research Scientist · Hamm Lab
Core researcher contributing to PAR4-driven platelet activation studies, PMP biology, and F2RL3 epigenetic characterization in estrogen-deficient models.
BB2
Benjamin Brown, MD, PhD
Computational Chemistry
Molecular dynamics, PAR4 binding modelling, and structure–activity relationship optimization. Supports lead optimization and selectivity profiling for the SEP-001 analog series.
JC
Jackson Cassada
Research Technician · Vanderbilt
In vitro and in vivo model execution, Dept. of Pharmacology, Vanderbilt University. 50% FTE dedicated to the Septagen program.
Exit Strategy

Septagen Fits the Profile of Assets Pharma Acquires Early

Nine strategic buyers with independent rationale spanning cardiovascular leaders and women's health acquirors. Target: $200–$300M upfront at IND + FIH submission — the outlicense trigger.

AstraZeneca
CV + Women's Health
Novartis
Cardiovascular
Bayer
CV + Women's Health
Pfizer
Cardiovascular
Organon
Women's Health
Roche
Precision Medicine
Lilly
CV + Inflammation
Astellas
Women's Health
Boehringer / Takeda
Cardiovascular
Target exit: $200–$300M upfront · post-IND + FIH submission · pre-Phase 3. ThromboRisk™ CDx adds 30–50% acquisition premium vs. drug-only asset. Comparable to preclinical and IND-stage cardiovascular and precision medicine acquisitions 2022–2024.
Precedent Transactions
Roche × Carmot
Pre-Clinical · Metabolic therapeutic
$2.7B
Pfizer × Nimbus
Phase II · Immunotherapy
$4.0B
BMS × Nektar
Phase I · Immunotherapy partnership
$1.85B
Boehringer × Sitryx
Preclinical · Immunometabolic
$500M+
Investment Opportunity

$10M Seed Round

$11M+ in prior NIH / Vanderbilt grant funding validates the science. $10M funds an 18-month runway to IND + FIH submission — the outlicense trigger. No Series A required.

$10M
SAFE · $30M Valuation Cap · 20% Discount · May 2026

$10M funds an 18-month sprint to IND + FIH submission. Both SEP-001 and ThromboRisk™ are outlicensed immediately upon submission. The partner funds and executes Phase 1 and all subsequent development. Septagen does not carry clinical-stage risk.

Use of Proceeds
  • $2.8M — Vanderbilt lab (lead optimization, BioVU epigenomic study, prospective human platelet cohort, F2RL3 validation)
  • $2.0M — IND-enabling studies (GLP tox, hERG, safety pharmacology, formulation)
  • $1.0M — ThromboRisk™ CDx (CLIA validation, all four assay tiers, AMA PLA code)
  • $0.6M — Regulatory affairs (pre-IND FDA meeting, IND prep, FIH protocol)
  • $0.8M — Operations & IP (patent prosecution: compound + CDx + indication)
  • $1.2M — Contingency reserve (12% · 18-month runway assured)
Key Deliverables
  • IND application submitted to FDA
  • FIH protocol filed for FDA review
  • ThromboRisk™ LDT launched — revenue generating
  • BioVU epigenomic study + human platelet cohort completed (months 3--12)
  • BioVU F2RL3 menopausal validation completed
  • Pre-IND FDA meeting completed (month 14–15)
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Visual Resources

Septagen at a Glance — Two Audiences, One Story

A full visual summary for each audience. Click any panel to view at full size.

Investor Summary
The Mechanism, Market & Moat — 10 Panels
PAR4 axis · Three-ring IP · $200–$300M exit
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Plain-English Guide
What We're Doing & Why — No Medical Degree Required
For patients, advocates & the curious
Explore the Science
Appendix

Glossary & Mechanism Diagrams

Reference material for readers outside platelet biology — plain-language definitions for the abbreviations used throughout this site, followed by two diagrams of the PAR4 mechanism.

Glossary of Terms
AHA
American Heart Association.
AKI
Acute Kidney Injury — a sudden loss of kidney function.
BMS
Bristol Myers Squibb — advanced a PAR4 antagonist through Phase 2 before externalizing the program.
CD41+/PS+
Platelet-derived markers (CD41 surface protein; phosphatidylserine exposure) used to count circulating microparticles.
CDx
Companion Diagnostic — a test that identifies which patients are likely to benefit from a specific drug.
CPT
Current Procedural Terminology — the billing code system used to reimburse a clinical test.
F2RL3
The gene that codes for the PAR4 receptor (Coagulation Factor II Receptor-Like 3).
FIH
First-in-Human — the first clinical study of a drug in human volunteers.
hsCRP / IL-6
High-sensitivity C-Reactive Protein and Interleukin-6 — blood markers of systemic inflammation.
IND
Investigational New Drug application — the FDA filing required before human trials can begin.
MACE
Major Adverse Cardiovascular Events — a composite endpoint of heart attack, stroke, and cardiovascular death.
NETosis
Neutrophil Extracellular Trap formation — an inflammatory process that contributes to clotting.
NK3 Antagonist
A newer non-hormonal menopause therapy class (e.g., fezolinetant/Veozah, elinzanetant/Lynkuet).
PAR1
Protease-Activated Receptor 1 — the platelet receptor targeted by the older antagonist vorapaxar.
PAR4
Protease-Activated Receptor 4 — the platelet receptor targeted by SEP-001.
PAR4-AI
PAR4 Activation Index — Septagen's measurement of how active a patient's PAR4 receptors are right now.
PK
Pharmacokinetics — how a drug is absorbed, distributed, and cleared by the body.
PMP
Platelet Microparticle — a small inflammatory, clot-promoting particle shed from an activated platelet.
POI
Premature Ovarian Insufficiency — when the ovaries stop functioning normally before age 40.
QD
Once-daily dosing (Latin quaque die).
Rho-Kinase / MLC Axis
A signaling pathway (Rho-associated Kinase acting on Myosin Light Chain) that contracts the platelet's internal skeleton and pinches off microparticles.
SNP
Single Nucleotide Polymorphism — a common, naturally occurring variation in a gene.
VTE
Venous Thromboembolism — a blood clot forming in a vein.
Mechanism Diagrams
Diagram A
From Vessel Injury to Clot Formation
A single injury triggers thrombin generation, which activates two platelet receptors in parallel. PAR1 fires fast and fades; PAR4 fires slower and stays on — and is the branch no approved therapy addresses.
Vessel Injury
Endothelial damage exposes collagen and tissue factor
→
Thrombin Generated
Coagulation cascade converts prothrombin to thrombin
→
PAR1 Activated
High-affinity, fast, transient signal
PAR4 Activated
Lower-affinity, slower, sustained signal — also triggered by Cathepsin G
→
Platelet Activation
Shape change; internal signaling begins
↓
Granule Release
Platelet Aggregation
PMP (Microparticle) Shedding
Fibrin Formation
↓
Clot Formation — the PAR4 branch contributes 3× more PMPs than PAR1, driving the thromboinflammatory burden no current therapy addresses (Hamm lab, PMID 23307185)
Diagram B
The Rho-Kinase / MLC Axis
Why PAR4 sheds more microparticles than PAR1: a contractile signaling pathway, downstream of PAR4, that physically pinches off the platelet membrane.
PAR4 Activation
↓
G 12/13 & Gq Coupling
↓
RhoA-GTP Activation
↓
Rho-Kinase (ROCK) Activation
↓
Myosin Light Chain (MLC) Phosphorylation
↓
Actomyosin Contraction & Cytoskeletal Remodeling
↓
Membrane Blebbing → PMP Shedding (3× PAR1) → Thromboinflammatory Loop
Why This Matters

PAR1 and PAR4 both activate platelets, but only the PAR4 branch drives this Rho-Kinase/MLC contractile cascade strongly enough to shed microparticles at scale — 3× the rate of PAR1 (Hamm lab, PMID 23307185).

Those microparticles carry 5–100× the procoagulant activity of a resting platelet, and deliver P-selectin, CXCL4, and CCL5 to vessel walls and immune cells — a self-amplifying inflammatory loop.

Vorapaxar, a PAR1 antagonist, leaves this entire pathway intact. SEP-001 targets PAR4 directly, addressing the branch responsible for the thromboinflammatory burden while preserving PAR1-mediated hemostasis.