in vivo pharmacology models in Neurovascular & Stroke

Stereotaxic injection of collagenase rapidly disrupts the vascular endothelium, inducing a reproducible hemorrhage with the formation of an intracerebral hematoma, accompanied by an inflammatory response and clear neurological deficits. This ICH model provides a valuable translational tool for assessing the efficacy of your drug candidates on bleeding, neuroinflammation, and neuroprotection. Depending on your needs, it also offers the possibility to evaluate the risk of rebleeding or the effectiveness of antidotes across a panel of reference anticoagulants and fibrinolytics.

Stereotaxic infusion of a predetermined volume of autologous blood into the striatum generates a reproducible hematoma, inducing increased intracranial pressure, brain toxicity, and an inflammatory response associated with clear neurological deficits. This model provides a reliable tool for evaluating the efficacy of your drug candidates on edema, inflammation, or neuroprotection, while eliminating potential biases linked to their effects on bleeding volume.

Stereotaxic infusion of a predetermined volume of autologous blood into the striatum generates a reproducible hematoma, inducing increased intracranial pressure, cerebral toxicity, and an inflammatory response associated with clear neurological deficits. This model is a reproducible tool for evaluating the efficacy of your molecules on edema, inflammation, or neuroprotection, eliminating potential biases related to their effect on bleeding volume.

Validated model available in rats.

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.

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.

This preclinical ischemic stroke model relies on a transient mechanical occlusion of the MCA (tMCAO), reproducing cerebral ischemia followed by controlled reperfusion. As a historical and extensively documented model, it produces both cortical and subcortical lesions, enabling the evaluation of a wide range of therapeutic strategies against a pharmacological reference, as well as detailed exploration of their effects on tissue evolution and on longterm sensorimotor and cognitive recovery.

Validated model available in mice and rats.

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.

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.

ICH induced by collagenase injection Stereotaxic injection of collagenase rapidly disrupts the vascular endothelium, inducing a reproducible hemorrhage with the formation of an intracerebral hematoma, accompanied by an inflammatory response and clear neurological deficits. This ICH model provides a valuable translational tool for assessing the efficacy of your drug candidates on bleeding, neuroinflammation, and neuroprotection. Depending on your needs, it also offers the possibility to evaluate the risk of rebleeding or the effectiveness of antidotes across a panel of reference anticoagulants and fibrinolytics.

Validated model available in rats

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.

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

Stereotaxic injection of collagenase rapidly disrupts the vascular endothelium, inducing a reproducible hemorrhage with the formation of an intracerebral hematoma, accompanied by an inflammatory response and clear neurological deficits. This ICH model provides a valuable translational tool for assessing the efficacy of your drug candidates on bleeding, neuroinflammation, and neuroprotection. Depending on your needs, it also offers the possibility to evaluate the risk of rebleeding or the effectiveness of antidotes across a panel of reference anticoagulants and fibrinolytics.

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.

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.

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.

ICH induced by collagenase injection Stereotaxic injection of collagenase rapidly disrupts the vascular endothelium, inducing a reproducible hemorrhage with the formation of an intracerebral hematoma, accompanied by an inflammatory response and clear neurological deficits. This ICH model provides a valuable translational tool for assessing the efficacy of your drug candidates on bleeding, neuroinflammation, and neuroprotection. Depending on your needs, it also offers the possibility to evaluate the risk of rebleeding or the effectiveness of antidotes across a panel of reference anticoagulants and fibrinolytics.

Validated model available in rats

Stereotaxic injection of collagenase rapidly disrupts the vascular endothelium, inducing a reproducible hemorrhage with the formation of an intracerebral hematoma, accompanied by an inflammatory response and clear neurological deficits. This ICH model provides a valuable translational tool for assessing the efficacy of your drug candidates on bleeding, neuroinflammation, and neuroprotection. Depending on your needs, it also offers the possibility to evaluate the risk of rebleeding or the effectiveness of antidotes across a panel of reference anticoagulants and fibrinolytics.

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

• In vitro model of hemostasis and coagulation

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.

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.

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.

The pulmonary embolism model induced by injection of autologous clots relies on preparing and injecting pre‑formed calibrated clots into the jugular vein to selectively obstruct the pulmonary arteries. This model reproduces the acute increase in pulmonary pressure observed in human clinical settings, along with significant stress on the right ventricle and secondary vascular remodeling. The severity of the condition can be adjusted based on the amount of thrombotic material used. Its strong reproducibility and rapid implementation make it suitable for quickly evaluating the efficacy of thrombolytic, vasodilatory, or cardioprotective treatments.

Rat model.

This preclinical ischemic stroke model relies on a transient mechanical occlusion of the MCA (tMCAO), reproducing cerebral ischemia followed by controlled reperfusion. As a historical and extensively documented model, it produces both cortical and subcortical lesions, enabling the evaluation of a wide range of therapeutic strategies against a pharmacological reference, as well as detailed exploration of their effects on tissue evolution and on longterm sensorimotor and cognitive recovery.

Validated model available in mice and rats.

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.

ICH induced by collagenase injection Stereotaxic injection of collagenase rapidly disrupts the vascular endothelium, inducing a reproducible hemorrhage with the formation of an intracerebral hematoma, accompanied by an inflammatory response and clear neurological deficits. This ICH model provides a valuable translational tool for assessing the efficacy of your drug candidates on bleeding, neuroinflammation, and neuroprotection. Depending on your needs, it also offers the possibility to evaluate the risk of rebleeding or the effectiveness of antidotes across a panel of reference anticoagulants and fibrinolytics.

Validated model available in rats

We offer studies tailored to your PK and Neuro-PK needs, covering various administration routes (subcutaneous, intraperitoneal, intravenous, oral, intranasal, etc.) in both acute and chronic treatment paradigms. The bioavailability of your molecules is quantified across different compartments—including blood, brain, cerebrospinal fluid, or any other tissue of interest. This approach provides reliable data to support decision-making and accelerate the development of your therapeutic candidates.

Available in mice, rats, and pigs.