subarachnoid hemorrhage

HLY78 (4-Ethyl-5-methyl-5,6-dihydro-[1,3]dioxolo[4,5-j]phenanthridine) targets the DIX domain of Axin, is an activator of the Wnt/β-catenin signaling pathway and can enhance Axin-LRP6 binding to promote Wnt signaling.

ML351 is a potent and selective inhibitor of human 15-lipoxygenase-1 (15 LOX)(IC50: 200 nM).

INT-777 (S-EMCA) is a potent, selective TGR5 agonist with an EC₅₀ of 0.82 μM. Following subarachnoid hemorrhage in rats, INT-777 inhibits NLRP5-ASC inflammasome-mediated neuroinflammation via the TGR3/cAMP/PKA signaling pathway. INT-777 exhibits multiple effects, including metabolic regulation, anti-inflammatory activity, cholagogue effects, and vascular protection. INT-777 can be used in research on diseases such as metabolic syndrome, non-alcoholic fatty liver disease, inflammatory bowel disease, and pulmonary arterial hypertension.

LSKL, INhibitor of Thrombospondin (TSP-1) is a TGF-β1 antagonist that inhibits the binding of TSP-1 to LAP and reduces renal interstitial fibrosis and liver fibrosis. LSKL can also inhibit subarachnoid fibrosis, prevent the occurrence of chronic hydrocephalus and improve long-term neurocognitive deficits after subarachnoid hemorrhage by inhibiting TSP-1-mediated TGF-β1 activity.

Methazolamide-D6 is intended for use as an internal standard for the quantification of methazolamide by GC- or LC-MS. Methazolamide (T0106) is a carbonic anhydrase inhibitor. It reduces intraocular pressure and cerebrospinal fluid flow in a rat model of glaucoma. Methazolamide (T0106) reduces electroshock-induced seizures in rats with an ED50 value of 19.2 mg/kg. It also inhibits production of reactive oxygen species (ROS) in a primary cortical neuron (PCN) cellular model of subarachnoid hemorrhage (SAH) and reduces cerebral edema in a mouse model of SAH.3 Methazolamide (T0106) is larvicidal, with a 50% larvicidal concentration (LC50) value of 724 ppm, but has no activity when administered in the diet to adult A. aegypti. Formulations containing methazolamide have been used in the treatment of glaucoma.

Tirilazad, a nonglucocorticoid 21-aminosteroid, serves to inhibit lipid peroxidation. It mitigates the effects of trauma-induced brain or spinal cord injury, as well as damage resulting from stroke, ischemia, and reperfusion injury. Additionally, Tirilazad exhibits antiviral properties against nCoV and offers neuroprotection in cases of ischemic stroke. It is also utilized in subarachnoid hemorrhage research [1] [2] [3].

Tat-QFNP12 is a peptide that combines a transcriptional transactivator (Tat) transmembrane domain with an inhibitor targeting the interaction between N-Myc downstream regulated gene 2 (NDRG2) and protein phosphatase Mg2+/Mn2+ dependent 1A (PPM1A). This compound effectively mitigates blood-brain barrier endothelial tight junction disruption caused by elevated levels of matrix metalloproteinase-9 (MMP-9), alleviates cerebral edema, and promotes spontaneous activity along with symmetric limb movement in a mouse model of subarachnoid hemorrhage induced by endovascular puncture. These benefits are observed at a dosage of 20 mg/kg.

Tirilazad mesylate hydrate is the hydrated form of Tirilazad mesylate, a nonglucocorticoid, 21-aminosteroid known for inhibiting lipid peroxidation. It is used to mitigate brain or spinal cord injury resulting from trauma, stroke, ischemia, and reperfusion injury and exhibits antiviral activities against nCoV. Additionally, Tirilazad mesylate is noted for its neuroprotective properties in ischemic stroke and is utilized in subarachnoid hemorrhage research [1] [2] [3].

LSKL TFA (H-Leu-Ser-Lys-Leu-NH2 TFA) is a LAP-TGFβ derivative and a TGF-β1 antagonist that can cross the blood-brain barrier, inhibits the binding of TSP-1 to LAP and reduces renal interstitial fibrosis and liver fibrosis, inhibits subarachnoid fibrosis by inhibiting TSP-1-mediated TGF-β1 activity, prevents the occurrence of chronic hydrocephalus and improves long-term neurocognitive deficits after subarachnoid hemorrhage.

TAT-QFNP12 is a peptide that inhibits NDRG2-PPM1A interaction, reduces Smad2/3 phosphorylation, decreases MMP-9 production in astrocytes, and mitigates blood-brain barrier disruption following subarachnoid hemorrhage (SAH).

TAT-QFNP12 acetate is a polypeptide that inhibits the binding of NDRG2-PPM1A and reduces the phosphorylation of Smad2/3, leading to a decrease in the production of MMP-9 in astrocytes and mitigating blood-brain barrier disruption following subarachnoid hemorrhage (SAH).