Heart Failure with Preserved Ejection Fraction (HFpEF)

HFpEF is a clinical syndrome of left ventricular diastolic dysfunction despite normal ejection fraction. Key drivers include metabolic comorbidities (obesity, diabetes), chronic inflammation, microvascular dysfunction, and myocardial fibrosis. Hallmarks comprise impaired relaxation, elevated filling pressures, concentric remodeling, and exercise intolerance, often with pulmonary congestion and edema. HFpEF predominantly affects elderly and female populations. These distinct features, coupled with limited therapies, make HFpEF a critical priority for preclinical model development.

7+
Validated Models
30+
Studies Completed
7
IND-Enabling Studies

Advantages

Our Advantages

Industry-leading capabilities for heart failure research

Standardized Doppler & PV-loop technique for diastolic function analysis.

Expertise in assessing diastolic dysfunction using standardized Doppler echocardiography (Pulsed-Wave + Tissue Doppler Imaging) and pressure-volume (PV) loop analysis for comprehensive hemodynamic profiling in HFpEF models.

Drug efficacy & IND-enabling studies.

Extensive experience in mature preclinical models and IND-enabling drug efficacy studies.

First-in-class HFpEF spontaneous model in market for speeding up efficacy studies.

Proprietary first-in-class spontaneous HFpEF model accelerating therapeutic efficacy evaluation.

Model Library

*Model has been used in IND-enabling studies

Case Studies

Case Studies & Validation Data

Explore our validated heart failure studies demonstrating the efficacy of various therapeutic interventions.

HFD+ANGII

Ang II dosed dependent HFpEF with HFD

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(A) Heart histology: HFD+Ang II groups show dose-dependent remodeling vs. HFD+Vehicle, including cardiac hypertrophy, coronary artery alteration, and interstitial fibrosis. (B) Survival curve: Both Ang II groups show dose-dependent mortality.

HFD+Ang II induces diastolic dysfunction.

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(A) Representative M-mode images comparing HFD+Vehicle vs. HFD+Ang II (1 mpk) at 4 weeks. (B) Echo data shows Ang II causes concentric hypertrophy (↑LVPW;d, ↑LVd Mass) with preserved EF, and impaired diastolic function (↓e', ↑E/e' ratio).

HFD+L-NAME

HFD+L-NAME induces cardiac remodeling and diastolic dysfunction.

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(A) Representative B-mode/Doppler images. (B) Compared to Chow Diet, HFD+L-NAME mice show impaired diastolic function (altered E/A, ↑E/e'), increased LVPW;d, preserved EF, and larger LA area*. Data: mean±SEM; *p<0.05, p<0.01,*p<0.001.

Systemic and cardiac effects of HFD+L-NAME.

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(A) Body weight increased progressively vs. control. (B) SBP and DBP were significantly elevated. (C) Exercise tolerance time was reduced (*). (D) Masson's trichrome staining shows interstitial fibrosis vs. in control.

Drug treatment in an HFD+L-NAME model.

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(A) 16-week study design. (B) Body weight during 28-day treatment for four groups. (C-E) At endpoint, disease model (G2) shows diastolic dysfunction (↑E/e', ↓e'), reduced exercise capacity, and ↑NT-proBNP vs. lean control (G1). Treatments (G3: DAPA, G4: TZP) improve these parameters (*p<0.05, p<0.01,*p<0.001).

SHM

SHM spontaneously develops obesity and hypertension

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(A) Body weight, Food intake and LDL-C: SHM. (B) SHM group shows consistently and significantly elevated systolic (SBP) and diastolic (DBP) blood pressure vs. control from weeks 9-16.

Echocardiographic features of SHM model.

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(A) Representative PSAX M-mode, PW Doppler, and TDI images. (B) Quantitative analysis shows SHM mice vs. C57BL/6J controls have preserved EF, increased LVPW;d and LVd Mass (hypertrophy), and impaired diastolic function (↓e', ↑E/e'*). Data: mean±SEM; *p<0.05.

DAPA and TZP treatment in SHM model.

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(A) Timeline: Treatment from weeks 15-20. (B) Body weight change. (C) Endpoint blood pressure. (D) Serial echocardiography for EF, E/e', MV e', and E/A. Groups: G1 (Vehicle), G2 (DAPA 3 mpk), G3 (TZP 10 nmol/kg). Data: mean±SEM.

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