PeptideDB

SUN11602

CAS: 704869-38-5 F: C26H37N5O2 W: 451.60

SUN11602 is a novel aniline compound with basic fibroblast growth factor-like activity.
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Bioactivity SUN11602 is a novel aniline compound with basic fibroblast growth factor-like activity.
Invitro SUN11602 prevents glutamate-induced neuronal death in primary cultures of rat cerebrocortical neurons. SUN11602 increases the levels of CALB1 gene expression in cerebrocortical neurons[1]. SUN11602 exerts protective effects on hippocampal neurons through activation of FGFR1 and increases CalB expression[2]. SUN11602 promotes neurite outgrowth of primarily cultured rat hippocampal neurons[3].
In Vivo In WT mice, SUN11602 increases the levels of newly synthesized Calb in cerebrocortical neurons and suppresses the glutamate-induced rise in intracellular Ca2+. This Ca2+-capturing ability of Calb allows the neurons to survive severe toxic conditions of glutamate[1]. Oral administration of SUN11602 at the midpoint of Aβ1-40 and ibotenate injections attenuate short-term memory impairment in the Y-maze test, as well as spatial learning deficits in the water maze task. In addition, the SUN11602 treatment inhibits the increase of peripheral-type benzodiazepine-binding sites (PTBBS),which are a marker for gliosis[3].
Name SUN11602
CAS 704869-38-5
Formula C26H37N5O2
Molar Mass 451.60
Appearance Solid
Transport Room temperature in continental US; may vary elsewhere.
Storage
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
Reference [1]. Murayama N, et al. SUN11602, a novel aniline compound, mimics the neuroprotective mechanisms of basic fibroblast growth factor. ACS Chem Neurosci. 2013 Feb 20;4(2):266-76. [2]. Murayama N, et al. SUN11602-induced hyperexpression of calbindin D-28k is pivotal for the survival of hippocampal neurons under neurotoxic conditions. Brain Res. 2015 Jan 12;1594:71-81. [3]. Ogino R, et al. SUN11602 has basic fibroblast growth factor-like activity and attenuates neuronal damage and cognitive deficits in a rat model of Alzheimer's disease induced by amyloid β and excitatory amino acids. Brain Res. 2014 Oct 17;1585:159-66.