MF 268
MF 268 is an orally active, blood-brain barrier-permeable acetylcholinesterase (AChE) inhibitor with an IC50 of 9 nM in rats. MF 268 binds to both the catalytic site and the regulatory anionic site of acetylcholinesterase, and increases the extracellular levels of acetylcholine, norepinephrine, dopamine and serotonin in the rat cortex via a dose-dependent pathway. MF 268 exhibits anti-amnesic effects in rats. MF 268 can be used in research related to Alzheimer's disease.
For research use only. We do not sell to patients.
- CAS No.: 154619-51-9
- Formula: C28H46N4O3
- Molecular Weight:486.70
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
-
Biological Activity
-
Chemical Information
- Protocols
- Purity & Documentation
- References
-
Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
AChE 9 nM (IC50) |
In Vitro
MF 268 (120 min) potently inhibits acetylcholinesterase from rat whole brain in vitro, with an IC50 of 9 nM[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MF 268 (0.5-2.0 mg/kg; s.c.; single dose) dose-dependently increases extracellular acetylcholine levels in the cortex of healthy rats, while moderately inhibiting cholinesterase[1].
MF 268 (50 μM; intracortical perfusion via microdialysis probe; continuous administration; 6 hr) increased extracellular ACh levels in the cortical cells of healthy rats by 5900%, while also altering the levels of NE, DA and 5-HT[1].
MF 268 (2-12 mg/kg; p.o.; single administration) exerts a persistent and selective reversal effect on Scopolamine (HY-N0296)-induced amnesia in rats, and the inhibition rate of whole-brain cholinesterase remains at 55% at 360 min after administration at 5 mg/kg[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Animal Model:Sprague-Dawley (male; 225-320 g for microdialysis; 170-190 g for cholinesterase activity assays)[1]
-
Dosage:0.5 mg/kg; 2.0 mg/kg; 5.0 mg/kg
-
Administration:p.o.; single dose
-
Result:Elevated cortical extracellular acetylcholine (ACh), peaking at 300 % (0.5 mg/kg), 460 % (2.0 mg/kg, 4 hr), 1200 % (5.0 mg/kg, 5.5 hr).
Attained maximal whole‑brain cholinesterase inhibition of 2.3 % (2.0 mg/kg, 9 hr) and 9.7 % (5.0 mg/kg, 12 hr).
Raised norepinephrine (NE) levels to 70 % (0.5 mg/kg), 100 % (2.0 mg/kg), 180 % (5.0 mg/kg).
Boosted dopamine (DA) levels to 70 % (0.5 mg/kg), 60 % (2.0 mg/kg), 100 % (5.0 mg/kg).
Maintained ACh and monoamine elevation ≥5 hr under 2.0 and 5.0 mg/kg doses.
Produced negligible serotonin (5‑HT) fluctuations across all doses.
Triggered mild cholinergic adverse events (chewing, tremor) exclusively at 5.0 mg/kg.
-
Animal Model:Sprague-Dawley (male; 225-320 g for microdialysis; 170-190 g for cholinesterase activity assays)[1]
-
Dosage:0.5 mg/kg; 2.0 mg/kg
-
Administration:s.c.; single dose
-
Result:Produced dose-dependent increases in extracellular cortical ACh with maximal increases of 360% (0.5 mg/kg at 5.5 hr) and 2500% (2.0 mg/kg at 5 hr), which remained elevated for at least 6 hr.
Achieved maximal whole-brain cholinesterase inhibition of 13% (0.5 mg/kg) and 41% (2.0 mg/kg).
Caused no consistent changes in NE levels with either dose.
Induced a transient increase in DA with the 0.5 mg/kg dose, while no DA change occurred with the 2.0 mg/kg dose.
Caused no major changes in 5-HT levels at either dose.
Induced slight cholinergic side effects (chewing, tremor) at both doses.
-
Animal Model:Wistar albino (male, ~300 g, scopolamine-induced amnesia)[2]
-
Dosage:2, 5 mg/kg (cholinesterase inhibition)
6, 8, 12 mg/kg (radial maze, locomotor activity) -
Administration:p.o.; single dose
-
Result:Exhibited an inverted U‑shaped dose‑response for reversing Scopolamine‑induced amnesia at 120 min pre‑test.
Maximally mitigated Scopolamine‑raised maze errors and completion time at 6 mg/kg.
Preserved baseline locomotion at 6, 8 mg/kg; counteracted Scopolamine‑triggered hypermotility at 12 mg/kg.
Reduced amnesic animal proportion to 16 % and lowered maze errors vs Scopolamine‑treated rats at 360 min pre‑test.
Delivered 55 % whole‑brain cholinesterase inhibition at 360 min post‑dose (30 % remaining at 15 h, 5 mg/kg).
Reached 22 % peak cholinesterase inhibition at 30 min post‑dose (18 % remaining at 15 h, 2 mg/kg).
Chemical Information
-
CAS No. 154619-51-9
-
Molecular Weight 486.70
-
Formula C28H46N4O3
-
SMILES
C[C@]12C=3C(N(C)[C@]1(N(C)CC2)[H])=CC=C(OC(NCCCCCCCCN4C[C@H](C)O[C@H](C)C4)=O)C3
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
-
Alzheimer’s Disease Modeling
Alzheimer’s Disease (AD) is a neurodegenerative disorder characterized by a progressive decline in cognitive functions and loss of specific types of neurons and synapses. Alzheimer's symptoms can be simulated in mice by injecting drugs (such as Aβ) or genetically modified.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
MF 268 Related Classifications
HY-105461 Related Classifications
Powered by Bioz