We provide robust and sensitive in vitro screening and characterization platforms for accelerating the discovery and screening of potential therapies for Amyotrophic Lateral Sclerosis (ALS). Our services are tailored to evaluate drug candidates using disease-relevant cellular models that reflect ALS-specific mechanisms. Key targets include mutant SOD1, TDP-43, FUS, and pathways associated with glutamate excitotoxicity, oxidative stress, and mitochondrial dysfunction. We assess pathological processes such as neuronal survival, protein aggregation, neuroinflammation, and cellular toxicity relevant to ALS progression.
Our in vitro efficacy testing services for ALS utilize a range of cell-based assays and mechanistic studies to evaluate therapeutic candidates. We offer high-content imaging, cytotoxicity assays, and biochemical analysis to provide comprehensive insights into the efficacy and mechanism of action of compounds. These methods enable detailed evaluation of therapeutic impact on ALS-relevant pathways and cellular processes.
Cell viability and cytotoxicity assays: Measure the survival and health of motor neurons and glial cells following compound treatment, providing critical information on drug safety and neuroprotection.
High-content imaging and analysis: Enables quantitative assessment of neuronal morphology, protein aggregation, and subcellular localization of disease-relevant proteins such as TDP-43 and SOD1.
Oxidative stress assays: Evaluate intracellular reactive oxygen species (ROS) production and antioxidant defense mechanisms, key factors in ALS pathology.
Mitochondrial function assays: Assess mitochondrial membrane potential, ATP production, and respiration to determine drug effects on cellular energy metabolism.
Glutamate excitotoxicity assays: Examine compound efficacy in preventing excitotoxic neuronal damage, a major contributor to ALS progression.
Inflammatory marker quantification: Measure cytokine release and glial activation to evaluate modulation of neuroinflammatory responses by therapeutic candidates.
We measure a diverse set of pharmacological and mechanistic parameters to determine drug efficacy, toxicity, and mechanism of action. These include cellular viability, protein aggregation, oxidative stress markers, mitochondrial health, and inflammatory responses. Accurate quantification of these parameters is critical for candidate selection and translational success.
Cell viability (EC50/IC50): Indicates the effective or inhibitory concentration of a compound required to achieve a specific response, essential for potency assessment.
Protein aggregation (inclusion counts, fluorescence intensity): Quantifies the reduction of pathological protein aggregates, important for disease modification.
Reactive oxygen species (ROS) levels: Evaluates oxidative stress mitigation, a key therapeutic goal in ALS.
Mitochondrial membrane potential and ATP levels: Measures improvements in cellular energy metabolism and mitochondrial integrity.
Cytokine release (e.g., TNF-α, IL-6): Assesses modulation of neuroinflammation, relevant for neuroprotective strategies.
Neurite outgrowth and morphology: Reflects neuronal health and potential for regeneration, important for functional recovery.
The 5-Hydroxytryptamine Receptor 1A (5-HT1A) modulates neuronal excitability and neuroprotection, playing a potential role in Amyotrophic Lateral Sclerosis (ALS) pathogenesis. Testing its function aids in identifying therapeutic targets and assessing drug efficacy. Key methods include receptor binding assays and functional signaling studies. Main parameters assessed are receptor expression, ligand affinity, and downstream signaling activity, providing critical insights for ALS drug development.
| Pharmacological Activity | Parameter |
|---|---|
| Serotonin 5-HT1A receptor affinity | Ki |
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