Services Portfolio

Servatrix Biomed S.L. – NRF2-Driven Preclinical Services

Servarix Biomed S.L. accelerates the path from discovery to clinic through advanced preclinical solutions focused on NRF2, the master regulator of oxidative stress, inflammation, and cellular homeostasis.

Our integrated approach combines mechanistic assays, in silico prediction tools, and translational in vivo models to deliver robust, reproducible, and clinically relevant data.

Why Choose Us

A compact, execution-focused partner combining mechanistic depth with translational endpoints and rigorous quality governance.

Accelerated proof-of-concept: pre-timed study packages and ready-to-start cohorts reduce timelines to 12–16 weeks.
In silico + wet-lab synergy: advanced AI predictions for ADME/DMPK and toxicity, selectively confirmed in laboratory.
Translational endpoints: integration of molecular, histopathological, and functional biomarkers tied to clinical relevance.
Quality and governance: reproducibility standards, curated data repositories, and milestone-based go/no-go decisions.

Service Portfolio

1. Mechanism of Action and NRF2 Target Engagement

Demonstrate the robust, specific activation of NRF2 by candidate compounds.

  • ARE-luciferase assays (EC50/IC50)
  • KEAP1/NRF2 protein-protein interaction assays (FP/AlphaScreen)
  • NRF2-dependent gene and protein expression profiling
  • Promoter occupancy confirmation (TransAM, ChIP-qPCR/ChIP-seq)

2. In Silico Redox Selectivity and Preliminary Safety

Early de-risking to flag promiscuous compounds and off-target liabilities.

  • ADME/DMPK predictions (permeability, stability, PPB, clearance)
  • AI-based toxicity alerts (hERG, CYP TDI, mitochondrial toxicity, etc.)
  • Compound scoring and go/no-go recommendations.

3. Cytoprotection under Oxidative Stress (In Vitro PoC)

Functional proof-of-concept across human and rodent cell systems.

  • Oxidative stress challenges (t-BHP/H₂O₂) in hepatocytes, SH-SY5Y neurons, retinal and cardiac cells.
  • Readouts: viability, ROS, apoptosis via flow cytometry and confocal microscopy.
  • Pharmacodynamics: NRF2-dependent genes and proteins (HMOX1, NQO1).

4. Accelerated Proof of Concept for MASH/NASH (12–16 weeks)

Translational in vivo efficacy integrating NRF2 pharmacodynamic biomarkers.

  • Endpoints: NAS (steatosis, inflammation, ballooning), fibrosis, ALT/AST, lipids, hepatic NRF2 biomarkers.
  • Animal models: STAM and choline-deficient variants (in collaboration with IIB “Sols-Morreale” CSIC-UAM).
  • Imaging: MRI for non-invasive hepatic/adipose metabolism assessment.

5. Proof of Concept in Neurodegeneration (Alzheimer’s & Parkinson’s)

Evaluate NRF2 contribution in translational neurodegenerative models.

  • Alzheimer’s: APP/TAU ± NRF2 models; pathology, neuroinflammation, and behavior.
  • Parkinson’s: MPTP and α-synuclein models; motor and nigrostriatal biomarkers.
  • CNS-NRF2 panel: integration of oxidative stress and inflammasome markers.

6. Systemic Inflammation and Inflammasome Analytics

Characterize NRF2 modulation across inflammatory processes.

  • In vitro & in vivo LPS activation in cells and mice; cytokine profiling.
  • Key biomarkers: caspase-1, IL-1β, IL-18; tissue-level NRF2 pharmacodynamics.
  • Deliverables: integrated cytokine profiles, mechanistic links to NRF2 activity.

Quality Framework

A compact, execution-focused partner combining mechanistic depth with translational endpoints and rigorous quality governance.

Accelerated proof-of-concept: pre-timed study packages and ready-to-start cohorts reduce timelines to 12–16 weeks.
In silico + wet-lab synergy: advanced AI predictions for ADME/DMPK and toxicity, selectively confirmed in laboratory.
Translational endpoints: integration of molecular, histopathological, and functional biomarkers tied to clinical relevance.
Quality and governance: reproducibility standards, curated data repositories, and milestone-based go/no-go decisions.

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