Stroke
Stroke is one of the top neurological complications worldwide and accounts for around 10.8 million deaths annually. This condition may also result in acute ischemia or hemorrhage in the brain leading to cell inflammation and death. Protheragen provides MyD88-targeted therapies development services to mitigate neuroinflammation and promote recovery, addressing ischemic and hemorrhagic stroke pathologies.
Overview of Stroke
Globally, stroke continues to be a major cause of mortality and morbidity. Both ischemic and hemorrhagic stroke are encompassed within the disease, along with acute neurological injury as its hallmark feature. There is ongoing work that highlights a potentially important role of post-stroke neuroinflammation MyD88 signaling as orchestrated by damage associated molecular patterns (DAMPs) that trigger TLRs and IL-1Rs signaling in microglia, astrocytes, and endothelial cells.
Pathogenesis of Stroke
The explanation for stroke relies on sterile type inflammation caused by the MyD88 dependent TLR/IL-1R pathways activated in microglia, astrocytes, and endothelial cells. DAMPs like HMGB1 and mtDNA are released after ischemia, and the ligands stimulate these receptors, leading to proficient activation of NF-κB/MAPK pathways. These pathways enhance release of proinflammatory cytokines such as TNF-α, IL-1β, and recruitment of neutrophils and monocytes while worsening BBB breakdown and neuronal death.
Fig.1 The underlying mechanism of MyD88's involvement in CIRI. (F. Jiang et al., 2024)MyD88-Targeted Therapeutic Development for Stroke
| Pharmacological Agent | Animal Model | Mechanism of Action | Development Stage |
| ApTLR#1R | CCA and MCA ligation of Mice | Bind to TLR4, avoiding the ligand Binding | Preclinical |
| Astaxanthin | Prechiasmatic cistern SAH | Inhibit the NFKB activity | Preclinical |
| Curcumin | Prechiasmatic cistern SAH | Targets TLR4, preventing TLR4 dimerization upon ligand binding | Preclinical |
| Melatonin | LPS induced neuro-inflammation | Inhibit the TLR 4 and MyD88 cascade | Preclinical |
| Progesterone | Prechiasmatic cistern SAH | Inhibit the MyD88 | Preclinical |
| ST2825 | / | Mimics and directly binds to the TIR domain on MyD88, preventing MyD88 homodimerization and further signaling | Preclinical |
| T6167923 | / | Mimics and directly binds to the TIR domain on MyD88, preventing MyD88 | Preclinical |
Disclaimer: Protheragen focuses on providing preclinical research services. This table is for information exchange purposes only. This table is not a treatment plan recommendation. For guidance on treatment options, please visit a regular hospital.
Our Services
Protheragen offers specialized services for MyD88-targeted therapeutic discovery and advanced disease models for stroke. Our integrated platform leverages neuro-specific in vitro and in vivo models to enable high-throughput screening and functional evaluation of MyD88 signaling modulators, focusing on post-stroke neuroinflammation and neuronal repair.
Therapeutic Discovery Platform for Stroke
Protheragen's MyD88 discovery platform for stroke targets the dysregulated innate immune crosstalk between microglia, astrocytes, and infiltrating immune cells. The platform accelerates preclinical validation of therapies that disrupt MyD88-dependent neuroinflammatory networks.
Disease Models Development for Stroke
Protheragen provides comprehensive preclinical modeling services for stroke, including cell-based models, organoid models, and animal models that replicate the neuroinflammatory and ischemic/hemorrhagic cascades, enabling mechanistic studies and therapeutic validation.
- Microglia-Neuron Co-Cultures
- BBB-on-a-Chip
- 3D Ischemic Brain Organoids
- Astrocyte-Microglia Interaction Systems
- Middle Cerebral Artery Occlusion (MCAO)
- Collagenase-Induced Intracerebral Hemorrhage
- Photothrombotic Stroke
- hCX3CR1-Humanized Mice
Protheragen rigorously advances MyD88-targeted therapies for stroke through a translational framework integrating disease model development, pharmacokinetics and drug safety evaluation, and investigator-initiated trials. Our end-to-end approach bridges preclinical neuroinflammatory insights to early clinical validation, accelerating therapeutic development for post-stroke neuroprotection and recovery.
If you are interested in our services, please don't hesitate to contact us.
References
- Ahmed, H., et al. "Role of Adaptor Protein Myeloid Differentiation 88 (Myd88) in Post-Subarachnoid Hemorrhage Inflammation: A Systematic Review." Int J Mol Sci 22.8 (2021).
- Jiang, F., et al. "Myd88 Inhibition Attenuates Cerebral Ischemia-Reperfusion Injury by Regulating the Inflammatory Response and Reducing Blood-Brain Barrier Damage." Neuroscience 549 (2024): 121-37.
All of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.