Size : | Price | Quantity | |
---|---|---|---|
10 mg | $55.00 | ||
50 mg | $225.00 |
FPS-ZM1 (945714-67-0) is a high-affinity RAGE (Receptor for Advanced Glycation End products) receptor antagonist (IC50 = 0.6 μM). It lowers levels of Aβ via binding to the V domain of RAGE and can block multiple mechanisms of Aβ40- and Aβ42-induced cellular stress in RAGE-expressing brain endothelium, neurons and microglia in vitro and in vivo.1,2 Can cross the BBB. In a rat model of intracerebral hemorrhage, FPS-ZM1 was able to attenuate blood-brain barrier and white matter fiber damage.3 FPS-ZM1 antagonism of RAGE was able to ameliorate inflammatory damage after acute intracerebral hemorrhage via downstream blockade of high mobility box-1(HMGB1) signaling.4 FPS-ZM1 has also been shown to impair breast cancer cell invasion and metastasis.5
References/Citations:
1) Deane et al. (2012), A multimodal RAGE-specific inhibitor reduces amyloid β-mediated brain disorder in a mouse model of Alzheimer disease; J. Clin. Invest. 122 1377
2) Hong et al. (2016), Effects of RAGE-Specific Inhibitor FPS-ZM1 on Amyloid-β Metabolism and AGEs-Induced Inflammation and Oxidative Stress in Rat Hippocampus ; Neurochem. Res. 41 1192
3) Yang et al. (2015), Receptor for advanced glycation end-product antagonist reduces blood-brain barrier damage after intracerebral hemorrhage; Stroke 46 1328
4) Li et al. (2015), Blockade of high mobility box-1 signaling via the receptor for advanced end-products ameliorates inflammatory damage after acute intracerebral hemorrhage; Neurosci. Lett. 609 109
5) Kwak et al. (2017), Targeting of RAGE-ligand signaling impairs breast cancer cell invasion and metastasis; Oncogene 36 155
Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee
FPS-ZM1 (945714-67-0) is a high-affinity RAGE (Receptor for Advanced Glycation End products) receptor antagonist (IC50 = 0.6 μM). It lowers levels of Aβ via binding to the V domain of RAGE and can block multiple mechanisms of Aβ40- and Aβ42-induced cellular stress in RAGE-expressing brain endothelium, neurons and microglia in vitro and in vivo.1,2 Can cross the BBB. In a rat model of intracerebral hemorrhage, FPS-ZM1 was able to attenuate blood-brain barrier and white matter fiber damage.3 FPS-ZM1 antagonism of RAGE was able to ameliorate inflammatory damage after acute intracerebral hemorrhage via downstream blockade of high mobility box-1(HMGB1) signaling.4 FPS-ZM1 has also been shown to impair breast cancer cell invasion and metastasis.5
References/Citations:
1) Deane et al. (2012), A multimodal RAGE-specific inhibitor reduces amyloid β-mediated brain disorder in a mouse model of Alzheimer disease; J. Clin. Invest. 122 1377
2) Hong et al. (2016), Effects of RAGE-Specific Inhibitor FPS-ZM1 on Amyloid-β Metabolism and AGEs-Induced Inflammation and Oxidative Stress in Rat Hippocampus ; Neurochem. Res. 41 1192
3) Yang et al. (2015), Receptor for advanced glycation end-product antagonist reduces blood-brain barrier damage after intracerebral hemorrhage; Stroke 46 1328
4) Li et al. (2015), Blockade of high mobility box-1 signaling via the receptor for advanced end-products ameliorates inflammatory damage after acute intracerebral hemorrhage; Neurosci. Lett. 609 109
5) Kwak et al. (2017), Targeting of RAGE-ligand signaling impairs breast cancer cell invasion and metastasis; Oncogene 36 155
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