Insights & Research

Effective in MI models, failed in HFpEF trials. The reason? Wrong model. Learn how to select the right HFpEF model (TAC, AngII, Multi-hit) targeting diastolic dysfunction and fibrosis, with E/e' echocardiography and Azan staining correlation analysis.

Effective in mice, failed in humans. Why? Prevent translational gaps in SSc drug discovery by choosing the right model (Bleomycin, HOCl, or Tsk) based on your drug's MOA. Includes a strategic decision matrix.

For researchers facing 'no reproducibility' or 'unexpected negative data' in preclinical studies. We explain failure causes from mismatch of model selection and evaluation systems, and introduce 3 re-evaluation strategies: STAM model, AI pathology, and PRO-C3.

'It worked in mice, but not in humans.' The key to crossing this valley of death is to evaluate with the same 'measure' as clinical trials. We explain how to utilize non-invasive biomarkers like FibroScan (CAP/VCTE), PRO-C3, and ELF score.

'Scores differ by evaluator', 'No reproducibility'. How does digital pathology analysis using AI (Deep Learning) solve the limitations of traditional subjective pathology scoring? We introduce the latest use cases of HALO/QuPath.

Following the FDA Modernization Act 2.0, interest in Organ-on-a-Chip (MPS) is skyrocketing. We explore its potential to replace animal models in fibrosis research, its current limitations, and the pragmatic 'Hybrid Strategy'.

Comprehensive analysis of major MASH acquisitions and partnerships in 2025. Detailed examination of GSK, Roche, and Novo Nordisk mega-deals, approvals, and the latest industry trends with interactive visualization.

Analysis of the latest trends in the IPF field in 2025. Visualizing a year of contrasts with Boehringer Ingelheim's first new approval in over a decade, United Therapeutics' Phase 3 success, and Pliant's discontinuation.

Unsure if a quote is fair? Struggling to choose the right CRO? Discover the key cost drivers of preclinical fibrosis studies and a 3-point checklist to ensure high-quality data and successful outsourcing.

Improve the success rate of IBD drug discovery by correctly selecting between DSS and TNBS models. We explain the benefits of Pre-validated DSS and endoscopic evaluation (MEICS).

The UUO model is key for CKD drug development. Reduce data noise and N-numbers with Microsurgery. A preclinical CRO perspective on precision and 3Rs.

Overcoming challenges in the Bleomycin IPF model. How Micro-Sprayer® technology and therapeutic dosing designs improve clinical predictability in preclinical trials.

Moving from 'Speed' to 'Clinical Relevance'. A comprehensive guide to selecting the right MASH preclinical models (GAN Diet, CDA-HFD, STAM™) based on Mechanism of Action (MoA) and translational value.

A step-by-step guide to the Hydroxyproline Assay for quantifying total collagen. Covers acid hydrolysis, colorimetric detection, troubleshooting tips for standard curves, and comparisons with LC-MS/MS.

A comprehensive guide to Picro-Sirius Red staining for fibrosis assessment. Covers principles, detailed protocol, comparison with Masson's Trichrome, and quantification tips.

Ofev/Esbriet only slow progression. Nerandomilast (Jascayd) showed add-on efficacy and won FDA approval in 2025. We decode the precision molecular design of PDE4B selectivity and the FIBRONEER-IPF data.

Resmetirom alone: 25% fibrosis improvement. Semaglutide: 37%. The majority DON'T improve. The answer? Combination therapy. We map out the optimal FGF21 + GLP-1 + THR-β combos for the Post-Monotherapy era.

Semaglutide's ESSENCE trial delivered 63% MASH resolution—but only 37% fibrosis improvement. Is 'Lose weight, cure liver' the whole truth? We explore the limits in Lean MASH and when to use Resmetirom instead.

Resmetirom was approved in 2024—the first MASH drug ever. But with ~25% fibrosis improvement, 75% of patients still need better options. What's the winning Post-Rezdiffra strategy? We decode the science of THR-β and MAESTRO-NASH.

Assessment methods determine the quality of fibrosis research. We explain the principles and tips of histological assessment (Sirius Red, Masson's Trichrome) and biochemical quantification (Hydroxyproline), as well as objective quantification using the latest AI image analysis.

The developmental program that builds fetal organs, when reactivated in adults, can trigger fibrosis. Why does 'Wnt reactivation' occur in mature tissue? We explore TGF-β crosstalk and the Wnt pathway's potential as a drug target.

TGF-β is the master switch of fibrosis, yet extremely difficult to target due to immunosuppression and cancer risk. We explore new approaches—non-canonical Smad pathways and integrin activation inhibitors—to selectively block fibrosis.

NF-κB sits at the heart of inflammation, but block it systemically and you cripple infection defense. How do you navigate this 'double-edged sword'? We explore next-gen strategies: selective IKK inhibition and tissue-specific targeting.

Why does fibrotic tissue 'self-worsen'? The answer lies in mechanosensors YAP/TAZ. Stiffness begets fibrosis, which begets more stiffness—this positive feedback loop is the new drug target. We explain the Hippo pathway as a therapeutic lever.

Explaining the duality of macrophages in fibrosis (M1: Inflammation, M2: Fibrosis/Repair). We introduce the roles of M2 subtypes (M2a/b/c), the switch mechanism in fibrosis progression/resolution, and their potential as therapeutic targets.

Chronic inflammation causes fibrosis—that's known. But WHEN is the 'tipping point'? We decode M1→M2 macrophage polarization, TGF-β duality, and EMT to identify the optimal timing for therapeutic intervention.

Inflammation is not just a defense response but a crucial step towards tissue repair. We explain the initiation of acute inflammation, the active "resolution" via SPMs (Specialized Pro-resolving Mediators) and Efferocytosis, and the mechanisms of transition to chronicity.

Why do anti-fibrotic drugs keep failing? The answer lies in controlling the myofibroblast. We systematically explain TGF-β signaling, mechanotransduction, and the 'Achilles heel' for targeted drug discovery.

Myofibroblasts—the executors of fibrosis—should disappear after wound healing. Why do they persist and worsen fibrosis? We explore their origins (resident, pericyte, EMT) and survival signals to identify drug targets.

We explain the mechanisms of Pirfenidone and Nintedanib, approved for Idiopathic Pulmonary Fibrosis (IPF), and the latest development trends of novel anti-fibrotic candidates for MASH and renal fibrosis currently in Phase 2/3 clinical trials.

Explaining the technical challenges of the UUO (Unilateral Ureteral Obstruction) model used in CKD research and the utility of the IRI (Ischemia-Reperfusion Injury) model for assessing renal function. Reducing variability through skilled microsurgery is key.

The Bleomycin pulmonary fibrosis model is the gold standard for IPF drug discovery. We explain solutions to its biggest challenges—"spontaneous resolution" and "variability"—using Micro-Sprayer technology for uniform administration and optimal study design.

Explaining the paradigm shift in research models following the nomenclature change from NASH to MASH. We discuss the limitations of traditional diet-induced models (duration, mild fibrosis) and introduce "Accelerated MASH Models" and objective fibrosis quantification methods based on the latest findings.

DSS and TNBS models are widely used in Ulcerative Colitis (UC) and Crohn's Disease (CD) research. We explain how to resolve challenges such as lot variability, technical inconsistency, and subjective evaluation through pre-validation and endoscopic (MEICS) assessment.

Biomarkers are essential for non-invasive evaluation of fibrosis. We explain the diagnostic value, prognostic ability, and limitations of major markers for lung (KL-6, SP-D), liver (Hyaluronic Acid, ELF Score), heart, and kidney.