2. Disease Areas
  3. Neurological, Eye or Ear Disease
  4. Nervous System Injury

Nervous System Injury

Injuries to the nervous system, including peripheral nerve injury (PNI) and central nervous system (CNS) injury, result from explosive blasts and can cause immediate or delayed mortality. Clinical manifestations often involve headache, vertigo, seizures, and altered mental status, with posttraumatic stress disorder commonly occurring in affected individuals.

 

Nervous System Injury (28):

Cat. No. Product Name CAS No. Purity Chemical Structure
  • HY-50722
    NNC 55-0396 357400-13-6 98.43%
    NNC 55-0396 (NNC 55-0396 dihydrochloride) is a blood-brain-barrier-permeable T-type Ca2+ channel inhibitor and pan-P450 inhibitor. NNC 55-0396 selectively inhibits T-type Ca2+ channels, suppresses HIF-1α expression and stability and inhibits Kv currents. NNC 55-0396 reduces brain infarct and attenuates neurological dysfunction. NNC 55-0396 inhibits the activity of multiple P450 enzymes. NNC 55-0396 (free base) can be used for the research of brain injury, hypertension, and glioblastoma.
    NNC 55-0396
  • HY-19667
    BMS-561392 611227-74-8
    BMS-561392 (BMS-561392) is a selective ADAM17(TACE) inhibitor. BMS-561392 inhibits TNF-α secretion by regulating signaling pathways such as p44 MAPK and NF-κB. BMS-561392 also affects the survival of central nervous system-related cells including oligodendrocytes and microglia. BMS-561392 promotes microglial apoptosis, enlarges the injury area and exacerbates astrogliosis in a mouse spinal cord injury model. BMS-561392 can be used in research related to spinal cord injury and inflammatory diseases.
    BMS-561392
  • HY-19667A
    BMS-561392 formate 2922280-85-9 99.13%
    BMS-561392 formate (DPC 333 formate) is a selective ADAM17(TACE) inhibitor. BMS-561392 formate inhibits TNF-α secretion by regulating signaling pathways such as p44 MAPK and NF-κB. BMS-561392 formate also affects the survival of central nervous system-related cells including oligodendrocytes and microglia. BMS-561392 formate promotes microglial apoptosis, enlarges the injury area and exacerbates astrogliosis in a mouse spinal cord injury model. BMS-561392 formate can be used in research related to spinal cord injury and inflammatory diseases.
    BMS-561392 formate
  • HY-N0745
    Senkyunolide I 94596-28-8 99.37%
    Senkyunolide I is an orally active, blood-brain barrier-permeable metabolite of Z-ligustilide (HY-N0401A). Senkyunolide I is isolated from Ligusticum chuanxiong. Senkyunolide I upregulates p-Erk1/2 and Nrf2/HO-1, and inhibits Caspase 3. Senkyunolide I alleviates Apoptosis. Senkyunolide I increases the pain threshold in mice and reduces acetic acid-induced writhing responses in mice. Senkyunolide I improves neurological deficits, reduces infarct volume and alleviates cerebral edema in rats with focal cerebral ischemia-reperfusion injury. Senkyunolide I protects renal function and structural integrity in a mouse model of renal ischemia-reperfusion injury. Senkyunolide I is applicable to research related to focal cerebral ischemia-reperfusion injury, migraine, and renal ischemia-reperfusion injury.
    Senkyunolide I
  • HY-N0663
    Talatisamine 20501-56-8 99.77%
    Talatisamine is an orally active cyclophilin D activator isolated from the roots of Aconitum carmichaeli Debx. Talatisamine exerts biological functions by activating cyclophilin D, inhibiting Ca2+-dependent opening of the mitochondrial permeability transition pore (mPTP) (IC50=78 μM), and blocking delayed rectifier K+ channels (IC50=146 μM). Talatisamine possesses both antioxidant and membrane-stabilizing properties, effectively inhibits lipid peroxidation and protects mitochondrial membrane function. Talatisamine exhibits multiple activities including antiarrhythmic, hypotensive, anti-inflammatory, anticancer and neuroprotective effects. Talatisamine finds applications in the research of ischemic diseases, rheumatoid arthritis, inflammation-related diseases and Alzheimer's disease.
    Talatisamine
  • HY-N0657
    Pinoresinol Diglucoside 63902-38-5 99.84%
    Pinoresinol Diglucoside is an orally active lignan with multifunctional bioactivity. Pinoresinol Diglucoside interacts with targets including ALB, HIF1A, GSK3B, BCL2, MARK3, IL6, NF-κB p65, Nrf2, HO-1, and TLR4, and modulates pathways including PI3K-Akt, estrogen, MAPK, Rap1, AKT/mTOR/NF-κB, and TGF-β1/Smads. Pinoresinol Diglucoside regulates osteogenesis, bone resorption, oxidative stress, inflammation, apoptosis, ferroptosis, ferritinophagy, cardiac fibrosis, and vasorelaxation. Pinoresinol Diglucoside can be used for the research of osteoporosis, ischemia/reperfusion-induced brain injury, Alzheimer’s disease, myocardial ischemia-reperfusion injury, chondrodysplasia, diabetic cardiomyopathy, cardiac hypertrophy, hypertension, cisplatin-induced hearing loss, atherosclerotic cardiovascular diseases, and disuse osteoporosis.
    Pinoresinol Diglucoside
  • HY-181126
    G194-0712 1029737-28-7
    G194-0712 is a selective histone deacetylase 5 (HDAC5) activator with an EC50 of 7.96 μM and a Kd of 2.53 μM. G194-0712 restores ACTN4-K417 deacetylation and nuclear import, and increases CSTA expression. G194-0712 accelerates wound closure in chronic wound models, reducing wound area and epithelial gap. G194-0712 can be used for the research of chronic skin wounds, such as diabetic wounds, ischemic wounds, radiation injury wounds.
    G194-0712
  • HY-P992422
    NG004
    NG004 is a fully human monoclonal antibody targeting Nogo-A. NG004 reduces retinal Nogo-A levels, blocks the binding of the Nogo-A-receptor complex, and neutralizes the Nogo-A protein. NG004 can be used in studies related to diabetic retinopathy, stroke and acute spinal cord injury.
    NG004
  • HY-180327
    NEPP11 313051-12-6
    NEPP11 is a cyclopentenone prostaglandin analogue. NEPP11 can inhibit glutamate-induced HT22 cell death in mouse hippocampus and prevent manganese-induced apoptosis in PC12 cells. NEPP11 can activate Nrf2 and maintain MEK1/2 and ERK1/2 activity by inhibiting c-Raf downregulation. NEPP11 exerts a neuroprotective effect in a mouse model of focal cerebral ischemia caused by permanent middle cerebral artery occlusion.
    NEPP11
  • HY-132187
    Sphingosylphosphorylcholine 1670-26-4 99.50%
    Sphingosylphosphorylcholine is a bioactive lipid and a major component of plasma high-density lipoprotein that binds to OGR1 with a Kd of 33.3 nM. Sphingosylphosphorylcholine triggers delayed phosphorylation of Smad2, upregulates α-SMA expression, and activates TRPM3. Sphingosylphosphorylcholine reduces Apoptosis and upregulates the expression of uPA and its receptor uPA-R. Sphingosylphosphorylcholine exerts anti-apoptotic, anti-cardiac hypertrophy and pro-wound healing effects. Sphingosylphosphorylcholine induces scratching behavior in mice. Sphingosylphosphorylcholine is used in studies related to atopic dermatitis, promyelocytic leukemia, heart failure, myocardial ischemia/reperfusion injury, ovarian cancer, breast cancer, pancreatic cancer, and skin wound healing disorders in genetically impaired healing diabetes.
    Sphingosylphosphorylcholine
  • HY-176803
    MF-DH-300 2673403-86-4 99.53%
    MF-DH-300 is a 15-PGDH inhibitor that can be applicable to the research of muscle disorders such as spinal muscular atrophy (SMA).
    MF-DH-300
  • HY-B0464A
    Hydralazine 86-54-4 99.94%
    Hydralazine is an orally active, blood-brain barrier-permeable DNA methyltransferase inhibitor with vasodilatory, arterial smooth muscle relaxant and hypotensive activities. Hydralazine reactivates silenced tumor suppressor genes via mediating DNA demethylation, while exerting neuroprotective and anti-inflammatory properties. Hydralazine inhibits NOS-2 (iNOS) and COX-2, and reduces the production of NO and PGEE2; meanwhile, Hydralazine scavenges reactive oxygen species and inhibits macrophage activation. Hydralazine alleviates motor dysfunction, neuropathic inflammatory pain, and formalin-induced somatic and emotional pain responses. In addition, Hydralazine directly induces DNA strand breaks and sister chromatid exchange, exhibiting certain mutagenic characteristics. Hydralazine has been widely used in studies on hypertension, various cancers (such as cervical cancer, leukemia), spinal cord injury and the mechanisms of inflammatory pain.
    Hydralazine
  • HY-11095
    NPS 2390 226878-01-9 99.90%
    NPS 2390 is an allosteric antagonist of calcium-sensing receptor (CaSR) and mGluR1/5. NPS 2390 inhibits the PI3K/Akt/mTOR signaling pathway, reduces hypoxia-induced intracellular calcium elevation, decreases the expression of autophagy (autophagy) proteins, regulates the expression of phenotypic marker proteins, and inhibits the proliferation of pulmonary artery smooth muscle cells. NPS 2390 attenuates the endogenous apoptosis (apoptosis) pathway, increases the expression level of Bcl-2, downregulates the expression levels of Bax, cytochrome c and caspase-3, alleviates cerebral edema and improves neurological function in rat models. NPS 2390 can be used in studies related to hypoxic pulmonary hypertension, traumatic brain injury, stroke and pain.
    NPS 2390
  • HY-N0385
    Gomisin J 66280-25-9 99.97%
    Gomisin J is a Schisandra chinensis-derived lignan that can inhibit multiple targets such as eNOS, AMPK (LKB1, CaMKIIβ), fetuin-A, NF-κB, Nrf2/HO-1, and can pass through the blood-brain barrier. Gomisin J increases NO bioavailability by activating eNOS, regulates lipid metabolism by activating the AMPK pathway, inhibits fetuin-A and NF-κB to exert anti-inflammatory effects, and activates Nrf2/HO-1 to enhance antioxidant capacity. Gomisin J has the activities of anti-hypertension, regulating liver lipid metabolism, and reducing cerebral ischemia-reperfusion injury, and can be used for research on hypertension, non-alcoholic fatty liver disease, cerebral ischemia-reperfusion injury, etc.
    Gomisin J
  • HY-B1016
    Trapidil 15421-84-8 98.0%
    Trapidil (AR-12008) is an orally active vasodilator and antiplatelet agent. Trapidil antagonizes platelet-derived growth factor (PDGF), inhibits phosphodiesterase, thromboxane A2 synthesis and pro-inflammatory cytokine production. Trapidil promotes prostacyclin biosynthesis, reduces lipid peroxidation, regulates nitric oxide metabolism, and inhibits cell proliferation and migration. Trapidil exerts tissue-protective effects, regulates bone turnover, and inhibits pyroptosis via the GPX3/Nrf2 pathway. Trapidil is applicable to research related to renal ischemia-reperfusion injury, chronic stable angina, restenosis, meningioma, diabetic cardiomyopathy and peripheral nerve crush injury.
    Trapidil
  • HY-N2000
    Bellidifolin 2798-25-6 99.74%
    Bellidifolin is an orally active compound with antiproliferative, anti-inflammatory and antioxidant properties. Bellidifolin modulates key signaling pathways including STAT3, PI3K-Akt, mTOR and BRD4, and inhibits the viral protein R (Vpr). Bellidifolin induces cell cycle arrest and apoptosis, exerts significant antifibrotic effects, and protects the heart, liver and nervous system. Bellidifolin is applicable to the research of various diseases such as lung cancer, non-alcoholic fatty liver disease, myocardial hypertrophy and ischemic cranial nerve injury.
    Bellidifolin
  • HY-P3281
    FGL peptide 499993-62-3 99.69%
    FGL peptide is a fibroblast growth factor receptor (FGFR) modulator and blood-brain barrier-penetrant. FGL peptide activates NCAM-FGFR and FGFR1 signaling pathways. FGL peptide alters expression of apoptosis, signal transduction and metabolism regulator genes in traumatic brain injury contexts. FGL peptide can be used for the research of traumatic brain injury.
    FGL peptide
  • HY-P99886
    Pexelizumab 219685-93-5 99.0%
    Pexelizumab (h5G1. 1-SC) is a humanized scFv monoclonal antibody directed against the C5 complement component. Pexelizumab inhibits apoptosis and leukocyte infiltration. Pexelizumab can be used for the research of cerebral IR injury and myocardial infarction.
    Pexelizumab
  • HY-103344
    ZJ43 723331-20-2 99.6%
    ZJ43 is a NAAG peptidase inhibitor and glutamate carboxypeptidase II/III (GCP II/III) inhibitor with human GCP II IC50 of 2.4 nM and Ki of 0.8 nM. ZJ43 blocks N-acetylaspartylglutamate hydrolysis, elevates extracellular N-acetylaspartylglutamate levels, and activates group II metabotropic glutamate receptors (mGluR). ZJ43 can be used for the research of schizophrenia, inflammatory pain, neuropathic pain, and traumatic brain injury.
    ZJ43
  • HY-106262
    Delcasertib 949100-39-4 98.21%
    Delcasertib (KAI-9803) is a potent and selective δ-protein kinase C (δPKC) inhibitor. Delcasertib (KAI-9803) could ameliorate injury associated with ischemia and reperfusion in animal models of acute myocardial infarction (MI).
    Delcasertib