Archives des Strokalliance - Page 2 of 3

tMCAO model by autologous clot injection

Injecting sizecalibrated autologous blood clots induces embolic occlusion of the proximal MCA segment. This model produces cortical and subcortical lesions similar to those observed in mechanical ischemia models. Mortality, deficit severity, and responsiveness to the reference fibrinolytic treatment (Alteplase) can be modulated by adjusting the amount of thrombotic material used for the embolic event. This original and wellcharacterized model enables the evaluation of a wide range of therapeutic strategies, together with longterm monitoring of functional recovery.

Validated model available in mice and rats.
ROTEM assay

This assay also allows investigation of compound interactions when combined with reference fibrinolytics (Alteplase, Tenecteplase).

The ROTEM assay, performed on fresh human whole blood, measures the viscoelastic properties of the clot throughout its formation and subsequent lysis.

A wide range of parameters can be extracted from the thromboelastogram, including the clotting time, the maximum clot firmness, and the 50% clot lysis time (LT50). This low-throughput assay offers an extensive and customisable set of hemostatic conditions for evaluating anticoagulant or thrombolytic compounds, including extrinsic or intrinsic activation pathways, as well as the addition of coagulation factors or modulators.
Glutamate-induced toxicity: organ-on-chip

Excitotoxicity is a key pathophysiological mechanism in ischemic stroke and contributes significantly to the consolidation of brain injury at sites distant from the ischemic core.

Our brain‑on‑chip model is designed to reproduce secondary excitotoxicity by delivering glutamate specifically into a synaptic chamber located at the interface between two spatially separated neuronal populations (i.e. each maintained in its own microphysiological environments).

Our microfluidic platform, combined with high‑content imaging, enables medium‑throughput screening of the effects of your compound on an isolated synapse, physically distant from the soma and exposed to excessive glutamate.
MCA occlusion by FeCl₃ or AlCl₃ application

This preclinical ischemic stroke model is induced by the formation of a platelet‑rich clot that is resistant to standard fibrinolytics (Alteplase, Tenecteplase) but responsive to other thrombolytic agents such as N‑acetylcysteine. By reflecting the subpopulation of patients who fail to respond to standard‑of‑care treatments, this translational model is a powerful tool for assessing the efficacy and superiority of your candidates, combination therapies, and pharmacological interactions.

Validated model available in mice.
ROTEM assay

The ROTEM assay, performed on fresh human whole blood, measures the viscoelastic properties of the clot throughout its formation and subsequent lysis. A wide range of parameters can be extracted from the thromboelastogram, including the clotting time, the maximum clot firmness, and the 50% clot lysis time (LT50). This low-throughput assay offers an extensive and customisable set of hemostatic conditions for evaluating anticoagulant or thrombolytic compounds, including extrinsic or intrinsic activation pathways, as well as the addition of coagulation factors or modulators.

This assay also allows investigation of compound interactions when combined with reference fibrinolytics (Alteplase, Tenecteplase).
MCA occlusion by thrombin injection in diabetic animals

This thrombotic model reproduces a highrisk clinical population, as diabetes increases lesion volumes as well as the occurrence and severity of hemorrhagic transformations. In this exclusive model, Alteplase loses its efficacy and can worsen ischemic damage. Fully aligned with STAIR recommendations, this comorbidityinclusive model is a key translational tool for evaluating the efficacy of your candidate alone or in combination, assessing associated hemorrhagic risk, and investigating pharmacological interactions.

Validated model available in mice.
Glutamate uptake by astrocytes

Astrocytes play a central role in maintaining synaptic homeostasis and preventing excitotoxicity by clearing excess extracellular glutamate. This protective function becomes impaired in reactive astrocytes during the post-ischemic inflammatory phase.

Our astrogliosis model enables the screening of your compounds targeting glutamate uptake in human astrocytes (iPSC) activated with a cytokines cocktail. Activation of the NFκB pathway is also available as a routine readout through our high-content imaging platform.
Tail bleeding assay

The tail bleeding test is a goldstandard assay used to evaluate hemostasis and platelet function in vivo.

This model is sensitive to anticoagulant and fibrinolytic treatments commonly administered in the clinic, such as heparin, direct oral anticoagulants, or Alteplase. This model supports the evaluation of candidate efficacy across multiple drug classes, such as anticoagulants, procoagulants, and antiplatelet agents.

Validated model available in mice