Ferroptosis Assay

Q: What is the typical lead time for a complete MoA (Mechanism of Action) validation?

Timelines vary based on the complexity of the Omics integration. Generally: Standard In Vitro Screening : 4–6 weeks. Deep MoA (Lipidomics + Target Validation) : 8–12 weeks. In Vivo Efficacy Studies : 12–16 weeks. Each project includes a dedicated project manager to provide bi-weekly updates.

Iron-Dependent Lipid Peroxidation-Driven Cell Death

Ferroptosis represents a paradigm shift in regulated cell death research, offering unprecedented opportunities for treating cancer, neurodegeneration, and ischemic injuries.

Ferroptosis is a unique form of regulated cell death characterized by iron dependency and catastrophic accumulation of lipid peroxides. Unlike apoptosis, ferroptosis can overcome drug resistance in cancer cells and modulate neurodegenerative disease progression.

Iron Metabolism
Dysregulated iron homeostasis drives oxidative stress and lipid peroxidation

GPX4 Pathway
Glutathione peroxidase 4 serves as the master regulator preventing lipid peroxidation

Therapeutic Potential
Dual applications in oncology (induction) and neuroprotection (inhibition)

Comprehensive Ferroptosis Drug Development Solutions

End-to-end services from early discovery to preclinical validation, tailored for biotech and pharmaceutical R&D teams.

Inhibitor/Inducer Screening

High-throughput and phenotypic screening platforms to identify novel ferroptosis modulators with optimized selectivity and potency profiles.

HTS and focused library screening
GPX4, System Xc-, FSP1, DHODH target-based assays
Cell viability and lipid peroxidation readouts
Structure-activity relationship (SAR) studies
Lead optimization with medicinal chemistry support

Target Discovery & Validation

Identify and validate novel ferroptosis regulators using multi-omics approaches and functional genomics technologies.

CRISPR/Cas9 genetic screening (whole-genome & focused)
Spatial transcriptomics for TME analysis
Single-cell RNA-seq & proteomics
Biomarker discovery (lipid peroxidation, iron metabolites)
Mechanism-of-action (MoA) elucidation

Drug Efficacy Evaluation

Rigorous in vitro and in vivo pharmacology studies to assess therapeutic potential and optimize drug candidates.

Multi-cancer cell line panels (>50 models)
Patient-derived xenograft (PDX) models
Neurodegenerative disease models (Alzheimer's, Parkinson's)
Dose-response and time-course studies
Combination therapy evaluation

Mechanism Studies

Deep mechanistic insights using cutting-edge analytical platforms to understand ferroptosis execution and drug action.

LC-MS/MS targeted & untargeted lipidomics
Real-time lipid peroxidation imaging
Iron quantification and redox state analysis
Metabolomics and pathway enrichment analysis

Advanced Analytical Platforms

Industry-leading technologies delivering unparalleled depth and precision in ferroptosis research and drug development.

Single-Cell Multiparametric Analysis

Simultaneous measurement of 40+ markers per cell
Lipid peroxidation & iron species detection
Immune cell profiling in TME
Ferroptosis pathway activation mapping
Drug response heterogeneity assessment
Rare population identification

Spatial Gene Expression Profiling

Whole-transcriptome spatial mapping
Tumor microenvironment architecture
Ferroptosis gradient visualization
Cell-cell interaction networks
Drug penetration & efficacy mapping
Niche-specific biomarker discovery

Comprehensive Lipid Profiling

1000+ lipid species identification
PUFA-containing phospholipids (PE, PC, PI)
Oxidized lipid (lipid hydroperoxide) quantification
Isotope tracing metabolic flux analysis
Temporal lipidome dynamics
Biomarker validation

Target Discovery & Validation

Genome-wide CRISPR knockout/activation screens
Focused ferroptosis gene panel screens
Single-cell RNA sequencing
Bulk RNA-seq with pathway analysis
Gene editing & stable cell line generation

Proprietary Model Library

Access our extensive collection of ferroptosis-sensitive cell lines and validated animal models, enabling rapid translation from discovery to preclinical validation.

Cancer Models

GPX4-low tumor cell lines (50+ types)
Therapy-resistant variants
PDX models
Syngeneic mouse models (melanoma, GBM, PDAC)

Neurodegeneration

Alzheimer's disease (5xFAD, APP/PS1)
Parkinson's disease (α-synuclein models)
Stroke & ischemia-reperfusion injury
ALS & spinal cord injury models

Organ Injury

Acute kidney injury (AKI) models
Drug-induced liver injury (DILI)
Cardiac ischemia-reperfusion
Sepsis-induced organ damage

Your Trusted Ferroptosis Research Partner

Combining scientific excellence, technological leadership, and commercial expertise to accelerate your therapeutic programs.

Specialized Knowledge

15+ years of dedicated research in regulated cell death pathways, led by a multidisciplinary team of PhD scientists.

Advanced Technology

State-of-the-art platforms for high-resolution spatial analysis and mass spectrometry, tailored for complex ferroptosis assays.

Accelerated Timelines

Streamlined workflows and established protocols reduce project timelines by 40%, ensuring faster go/no-go decisions.

Comprehensive Service Portfolio

A seamless transition through the development pipeline, offering total project oversight from discovery to IND filing.

FAQ

1. How do you differentiate Ferroptosis from other forms of regulated cell death (RCD) in drug screening?

Distinguishing ferroptosis from apoptosis, necroptosis, or autophagy is critical for MoA validation. Our platform employs a multi-parametric approach:

Pharmacological Rescue: We use specific inhibitors like Ferrostatin-1 (Fer-1) or Liproxstatin-1 to confirm that cell death is specifically iron-dependent.
Morphological Analysis: Using Transmission Electron Microscopy (TEM), we look for the "gold standard" hallmarks: shrunken mitochondria, increased membrane density, and loss of mitochondrial cristae, without the chromatin condensation typical of apoptosis.
Biochemical Profiling: We monitor the absence of Caspase-3 cleavage to rule out classical apoptosis.

2. Why is LC-MS/MS lipidomics essential for our ferroptosis project?

While fluorescent probes like C11-BODIPY provide a general readout of lipid peroxidation, they lack molecular specificity. Our LC-MS/MS platform identifies the exact lipid species being oxidized—specifically targeting arachidonic acid (AA)- and adrenic acid (AdA)-containing phosphatidylethanolamines (PEs). This provides high-resolution data necessary for IND filings and precise target engagement studies.

3. Can your platform support high-throughput screening (HTS) for synergistic effects with immunotherapy?

Yes. Ferroptosis is known to enhance tumor immunogenicity. We offer co-culture models (Tumor cells + T-cells/Macrophage) combined with Spatial Transcriptomics to analyze how your ferroptosis inducers modulate the Tumor Microenvironment (TME) and promote "cold-to-hot" tumor conversion.

4. What types of Ferroptosis-related animal models are available in your repository?

We maintain a robust library of models validated for ferroptosis research, including:

GPX4-deficient or ACSL4-overexpressing cell-derived xenografts (CDX).
Ischemia-Reperfusion Injury (IRI) models (Kidney and Heart) for testing ferroptosis inhibitors.
Neurodegenerative models (AD/PD) focused on iron accumulation in the substantia nigra or hippocampus.
NAFLD/NASH models to study lipid metabolism-driven cell death.

5. What is the typical lead time for a complete MoA (Mechanism of Action) validation?

Timelines vary based on the complexity of the "Omics" integration. Generally:

Standard In Vitro Screening: 4–6 weeks.
Deep MoA (Lipidomics + Target Validation): 8–12 weeks.
In Vivo Efficacy Studies: 12–16 weeks. Each project includes a dedicated project manager to provide bi-weekly updates.