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Dizocilpine Maleate [(+)-MK 801 maleate]

Alias: Dizocilpine;MK801; MK 801; MK-801;DIZOCILPINE MALEATE; (+)-MK-801 hydrogen maleate; Dizocilpine maleate [USAN]; 6LR8C1B66Q; DTXSID2045785; DIZOCILPINE MALEATE; 77086-22-7; (+)-MK 801 Maleate; (+)-MK-801 hydrogen maleate; Dizocilpine hydrogen maleate; Dizocilpine maleate [USAN]; UNII-6LR8C1B66Q; 6LR8C1B66Q; (+)-MK 801 hydrogen maleate; MK 801 Maleate
Cat No.:V1083 Purity: ≥98%
Dizocilpine Maleate [formerly (+)-MK-801)], the maleate salt of(+)dizocilpine,is a non-competitive antagonist of NMDA (N-Methyl-D-aspartate) receptors with a Kd of 37.2 nM in rat brain membranes.
Dizocilpine Maleate [(+)-MK 801 maleate]
Dizocilpine Maleate [(+)-MK 801 maleate] Chemical Structure CAS No.: 77086-22-7
Product category: GluR
This product is for research use only, not for human use. We do not sell to patients.
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Other Forms of Dizocilpine Maleate [(+)-MK 801 maleate]:

  • (-)-Dizocilpine Maleate [(-)-MK 801 maleate]
  • (Rac)-Dizocilpine ((Rac)-MK-801)
  • Dizocilpine (MK-801)
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Purity & Quality Control Documentation

Purity: ≥98%

Product Description

Dizocilpine Maleate [formerly (+)-MK-801)], the maleate salt of (+)dizocilpine, is a non-competitive antagonist of NMDA (N-Methyl-D-aspartate) receptors with a Kd of 37.2 nM in rat brain membranes. (+)-MK-801 acts as a potent anti-convulsant and likely has dissociative anesthetic properties, but it is not used clinically for this purpose due to the discovery of brain lesions, called Olney's lesions in test rats.

Biological Activity I Assay Protocols (From Reference)
Targets
NMDA Receptor
ln Vitro
In rat cerebral cortical membranes, [3H]dizocilpine maleate binds with NMDA receptors at a Kd of 37.2±2.7 nM[1]. N-Me-D-Asp-induced current blockade is progressive and long-lasting when dizocilpine maleate is used[3]. The NMDA-induced current is gradually suppressed by dizocilpine maleate. Even when Dizocilpine (MK-801) is applied for an extended period of time in the presence of NMDA, Mg2+ (10 mM) inhibits Dizocilpine from blocking the N-Me-D-Asp-induced current. In outside-out patches, dizocilpine inhibits NMDA-activated single-channel activity[3]. Dizocilpine maleate (less than 500 μM) suppresses LPS-induced microglia activation, which is accompanied by elevated Cox-2 protein expression in BV-2 cells. In BV-2 cells, dococilpine (MK-801; <500 μM) decreases microglial TNF-α production with an EC50 of 400 μM[4].
ln Vivo
In animal modeling, dizocilpine maleate can be used to create models of schizophrenia. Recent research suggests that drug-related memories are reactivated after exposure to environmental cues and may undergo reconsolidation, a process that can strengthen memories. Conversely, reconsolidation may be disrupted by certain pharmacological agents such that the drug-associated memory is weakened. Several studies have demonstrated disruption of memory reconsolidation using a drug-induced conditioned place preference (CPP) task, but no studies have explored whether cocaine-associated memories can be similarly disrupted in cocaine self-administering animals after a cocaine priming injection, which powerfully reinstates drug-seeking behavior. Here we used cocaine-induced CPP and cocaine self-administration to investigate whether the N-methyl-D-aspartate receptor antagonist (+)-5methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801) given just prior to reactivation sessions would suppress subsequent cocaine-primed reinstatement (disruption of reconsolidation). Systemic injection of MK-801 (0.05 or 0.20 mg/kg administered intraperitoneally) in rats just prior to reactivation of the cocaine-associated memory in the CPP context attenuated subsequent cocaine-primed reinstatement, while no disruption occurred in rats that did not receive reactivation in the CPP context. However, in rats trained to self-administer cocaine, systemic administration of MK-801 just prior to either of two different types of reactivation sessions had no effect on subsequent cocaine-primed reinstatement of lever-pressing behavior. Thus, systemic administration of MK-801 disrupted the reconsolidation of a cocaine-associated memory for CPP but not for self-administration. These findings suggest that cocaine-CPP and self-administration do not use similar neurochemical processes to disrupt reconsolidation or that cocaine-associated memories in self-administering rats do not undergo reconsolidation, as assessed by lever-pressing behavior under cocaine reinstatement conditions [5].
The effects of five administrations (3- to 4-day intervals) of morphine (MOR: 10 and 20 mg/kg, s.c.) alone, MK-801 (dizocilpine: 0.03, 0.1, 0.3 and 1 mg/kg, i.p.) alone, and combinations of MOR with MK-801 on the ambulation in mice were investigated. MK-801 at 0.3 and 1 mg/kg, but not at 0.03 and 0.1 mg/kg, significantly increased the ambulation of mice. Although the mice given repeated administrations of MK-801 (0.3 and 1 mg/kg) exhibited enhancement and reduction, respectively, in the ambulation-increasing effect of the individual doses, they showed significantly higher sensitivity than the saline-treated mice to the challenge with MOR (10 mg/kg). The repeated administrations of MOR (10 and 20 mg/kg) induced a progressive enhancement of the ambulation-increasing effect. The mice repeatedly given MOR (10 mg/kg) exhibited significant increase in the sensitivity to MK-801 (0.03-0.3 mg/kg). The coadministrations of MOR with MK-801 intensified the ambulation-increasing effect, and repeated coadministrations induced progressive enhancement of the effect, except for the combinations of MOR (10 or 20 mg/kg) with MK-801 (1 mg/kg). However, the induction of MOR sensitization was not modified by any doses of MK-801, except for the case of combination of MOR (20 mg/kg) with MK-801 (1 mg/kg) which was highly toxic (i.e., eliciting death or a moribund condition). On the other hand, simultaneous treatment with SCH 23390 (0.05 mg/kg, s.c.) or nemonapride (0.05 mg/kg, s.c.), or 4-hr pretreatment with reserpine (1 mg/kg, s.c.) strongly, and 4-hr pretreatment with alpha-methyl-p-tyrosine (200 mg/kg, i.p.) partially reduced the ambulation-increasing effect of both MOR (10 mg/kg) and MK-801 (0.3 mg/kg). Simultaneous treatment with naloxone (1 mg/kg, sc) selectively reduced the effect of MOR. However, simultaneous treatment with apomorphine (0.1 mg/kg, s.c.) did not modify the effects of either drug. These results suggest that the characteristics of the ambulation-increasing effects of MOR and MK-801 are similar to each other, and that the repeated treatments with MK-801 induce a cross-sensitization to MOR and vice versa[6].
Enzyme Assay
The compound MK-801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d] cyclohepten-5,10-imine maleate)] is a potent anticonvulsant that is active after oral administration and whose mechanism of action is unknown. We have detected high-affinity (Kd = 37.2 +/- 2.7 nM) binding sites for [3H]MK-801 in rat brain membranes. These sites are heat-labile, stereoselective, and regionally specific, with the hippocampus showing the highest density of sites, followed by cerebral cortex, corpus striatum, and medulla-pons. There was no detectable binding in the cerebellum. MK-801 binding sites exhibited a novel pharmacological profile, since none of the major neurotransmitter candidates were active at these sites. The only compounds that were able to compete for [3H]MK-801 binding sites were substances known to block the responses of excitatory amino acids mediated by the N-methyl-D-aspartate (N-Me-D-Asp) receptor subtype. These comprised the dissociative anesthetics phencyclidine and ketamine and the sigma-type opioid N-allylnormetazocine (SKF 10,047). Neurophysiological studies in vitro, using a rat cortical-slice preparation, demonstrated a potent, selective, and noncompetitive antagonistic action of MK-801 on depolarizing responses to N-Me-D-Asp but not to kainate or quisqualate. The potencies of phencyclidine, ketamine, SKF 10,047, and the enantiomers of MK-801 as N-Me-D-Asp antagonists correlated closely (r = 0.99) with their potencies as inhibitors of [3H]MK-801 binding. This suggests that the MK-801 binding sites are associated with N-Me-D-Asp receptors and provides an explanation for the mechanism of action of MK-801 as an anticonvulsant[1].
Cell Assay
Neurons were dissociated from the visual cortex of 2- to 6-day-old Long Evans rat pups and grown in culture for 5-43 days as described (21). Currents activated by excit-fory amino acids were measured in the whole-cell and outside-out patch-clamp configurations. Pipettes contained an internal solution (in mM) of 120 cesium methanesulfonate, 5 CsCI, 10 Cs2EGTA, 5 Mg(OH)2, 5 MgATP, 1 Na2GTP, and 10 Hepes (pH adjusted to 7.4 with CsOH). The external solution (in mM) was 160 NaCl, 2 CaC12, and 10 Hepes (pH 7.40). In whole-cell experiments, 300 nM tetrodotoxin and 10 kLM bicuculline methiodide were added to the external solution to suppress spontaneous activity. MK-801, the kind gift of Paul Anderson, was added from stock solutions of 2-50 mM in ethanol, stored at - 20'C. Final concentrations of ethanol were <0.1%. Cells or patches were bathed in control or agonist-containing external solution flowing from one of a linear array of 7-10 microcapillary tubes fed by gravity. Rapid solution changes were made by moving the array of tubes relative to the cell (whole-cell) or by moving the pipette relative to the tubes (patch). All experiments were done at 20-250C[3].
Animal Protocol
Systemic injection of Dizocilpine/MK-801 (0.05 or 0.20 mg/kg administered intraperitoneally) in rats just prior to reactivation of the cocaine-associated memory in the CPP context attenuated subsequent cocaine-primed reinstatement, while no disruption occurred in rats that did not receive reactivation in the CPP context. However, in rats trained to self-administer cocaine, systemic administration of MK-801 just prior to either of two different types of reactivation sessions had no effect on subsequent cocaine-primed reinstatement of lever-pressing behavior. Thus, systemic administration of MK-801 disrupted the reconsolidation of a cocaine-associated memory for CPP but not for self-administration. These findings suggest that cocaine-CPP and self-administration do not use similar neurochemical processes to disrupt reconsolidation or that cocaine-associated memories in self-administering rats do not undergo reconsolidation, as assessed by lever-pressing behavior under cocaine reinstatement conditions.[5]
Subjects [5]
Male Sprague-Dawley and Long-Evans Hooded rats weighing 280–350 g at the start of the experiment were housed in a temperature- and humidity-controlled colony room with a 12-h light/dark cycle (lights on at 6:00 a.m.). Sprague-Dawley rats were used for all CPP studies, and our initial self-administration studies used Long-Evans rats because of their higher general activity levels and thus higher initial lever pressing during acquisition of the self-administration task. However, to ensure that there were no strain differences in the effects of Dizocilpine/MK-801 on self-administration behavior, we also used Sprague-Dawley rats to test the effects of the highest dose of MK-801 compared with Saline vehicle in this strain. No significant differences were found for the effects of MK-801, so the data from both strains were pooled. Animals undergoing self-administration were housed in a 12-h reverse light/dark cycle (lights on at 6:00 p.m.). Experiments were conducted according to the National Institutes of Health Guide for the Care and Use of Laboratory Animals, and experimental protocols were approved by the University Animal Care and Use Committee. Animals were housed two per cage for the CPP studies and individually for the self-administration studies. Food and water were provided ad libitum except for when animals were engaged in experiments.
Drug administration [5]
Dizocilpine(+)-MK-801 hydrogen maleate was dissolved in sterile saline for i.p. injection (1 mL/kg). The doses chosen were 0.05 and 0.20 mg/kg, based on previous work by Przybyslawski and Sara (1997).
Surgery [5]
Self-administration surgery was conducted according to a modification of McFarland and Kalivas (2001). Rats were anesthetized with zyket (ketamine 87 mg/kg + xylazine 13 mg/kg) given intramuscularly prior to implanting a chronic indwelling i.v. catheter. The catheter was surgically implanted into the right jugular vein, and the distal end was led subcutaneously to the back between the scapulas. Catheters were constructed from Silastic tubing (9 cm; inner diameter 0.025 in, outer diameter 0.047 in) connected to a back-mount cannula pedestal, a bent 22-gauge metal cannula encased within a plastic screw connector attached to a polyester mesh (Plastics One). A small ball of silicone sealant was placed ∼2.8 cm from the end of the catheter. The right jugular vein was isolated, the most anterior portion of the vein was tied shut, and a small incision was made. The distal end of the catheter was inserted into the vein until the silicone ball was flush with the vein. The vein was secured by tying suture thread on both sides of the silicone ball; additionally, the thread on both sides was tied together. Immediately after surgery, the catheter was injected with 0.1 mL of locking solution: heparin (500 U/mL), gentamicin (5 mg/mL), and glycerol (60%) in sterile saline. Incisions were sutured, and the animal was given 5–7 d to recover. After surgery, the catheter was flushed daily with 0.1 mL of heparin (10 U/mL) and gentamicin antibiotic (5 mg/mL) in sterile saline to help protect against infection and catheter occlusion.
Behavioral procedures [5]
CPP [5]
All CPP studies were conducted during the same time of day. The proposed studies employed a three-compartment CPP apparatus as previously described (Brown et al. 2007). Briefly, the procedure consisted of a preconditioning preference test, training for 8 d (4 saline pairings alternating with 4 cocaine pairings), testing for CPP acquisition followed by extinction sessions, and cocaine-primed reinstatement with a 10 mg/kg, i.p. dose of cocaine (Brown et al. 2007). Except for the training days, rats had access to all three compartments of the CPP apparatus.

In Experiment 1, we tested whether Dizocilpine/MK-801 would impair reconsolidation of the memory for the cocaine-associated context during reinstatement testing. Animals underwent preconditioning, conditioning, testing, and extinction as described above, and on Reactivation Day 1, rats received saline or MK-801 (0.05 mg/kg or 0.20 mg/kg, i.p.) 30 min prior to a cocaine injection (10 mg/kg, i.p.) and placed immediately into the central compartment of the CPP box (Reactivation Day 1). Rats were allowed to explore all three compartments. The next day, the procedure from Reactivation Day 1 was repeated (Reactivation Day 2). This procedure was given for 2 d because our previous studies using a different pharmacological agent (Brown et al. 2007) indicated that one day of memory reactivation was not sufficient to disrupt subsequent cocaine-primed reinstatement. The following day, animals were tested for cocaine-primed reinstatement without any prior injection of either saline or MK-801 before being placed into the CPP box (Reinstatement Day). Rats were allowed to explore all three compartments.

Experiment 2 was identical to Experiment 1 with the exception of the cage location where Dizocilpine/MK-801 and cocaine injection took place on Reactivation Days 1 and 2. In Experiment 2, animals were given saline or MK-801 followed by cocaine 30 min later in the home cage instead of in the CPP apparatus for the two days of “reactivation.” This was done to determine whether reactivation of the memory for the cocaine-associated context by cocaine in the CPP context was necessary for the ability of MK-801 to disrupt reconsolidation. Animals underwent preconditioning, conditioning, testing, and extinction as described above but animals were injected with saline or MK-801 (0.20 mg/kg, i.p.) 30 min prior to a cocaine injection (10 mg/kg, i.p.) in the home cage. Animals remained in the home cages, and the next day, the procedure from the first day of reactivation was repeated. The following day, animals were tested for cocaine-primed reinstatement in their CPP box without any prior microinjection of saline or MK-801, exactly as described for the Reinstatement Day in Experiment 1 above.
Dissolved in saline; 0.1mg/kg; oral gavage
Male Sprague-Dawley rats
ADME/Pharmacokinetics
Dizocilpine (MK-801) is a non-competitive NMDA receptor antagonist with high binding affinity, requiring an open channel for receptor blockade. Key pharmacokinetic characteristics include:
1. Bioavailability & Absorption
o While specific bioavailability data for dizocilpine is not provided in the sources, its structural analog orphenadrine (an NMDA antagonist with similar properties) demonstrates blood-brain barrier penetration, suggesting dizocilpine may share this trait.

2. Metabolism & Elimination
o Studies on reeler mice indicate dizocilpine’s efficacy correlates with GABAergic modulation, implying potential hepatic metabolism involving neurotransmitter pathways.
o Comparative pharmacokinetic data from paliperidone derivatives suggest rapid metabolism may occur for certain CNS-targeting drugs, though dizocilpine’s exact metabolic profile remains unspecified.

3. Pharmacodynamic Interactions
o Dizocilpine’s NMDA receptor blockade is enhanced in models of synaptic plasticity dysfunction, suggesting context-dependent pharmacokinetic-pharmacodynamic relationships.
For precise quantification (e.g., Tmax, half-life), additional data beyond the current search results would be required.
Toxicity/Toxicokinetics
mouse LD50 intravenous 30 mg/kg United States Patent Document., #5273989
References

[1]. The anticonvulsant MK-801 is a potent N-Me-D-Asp antagonist. Proc Natl Acad Sci U S A. 1986 Sep;83(18):7104-8.

[2]. Convergent Strategy to Dizocilpine MK-801 and Derivatives. J Org Chem. 2018 Apr 6;83(7):4264-4269.

[3]. Block of N-Me-D-Asp-activated current by the anticonvulsant MK-801: selective binding to open channels. Proc Natl Acad Sci U S A. 1988 Feb;85(4):1307-11.

[4]. MK-801 and dextromethorphan block microglial activation and protect against neurotoxicity. Brain Res. 2005 Jul 19;1050(1-2):190-8.

[5]. The NMDA antagonist MK-801 disrupts reconsolidation of a cocaine-associated memory for conditioned place preference but not for self-administration in rats. Learn Mem. 2008 Dec 2;15(12):857-65.

[6]. Modification by MK-801 (dizocilpine), a noncompetitive NMDA receptor antagonist sensitization: evaluation by ambulation in mice. Nihon Shinkei Seishin Yakurigaku Zasshi. 1996 Feb;16(1):11-8.

[7]. Decrease of growth and differentiation factor 10 contributes to neuropathic pain through N-Me-D-Asp receptor activation. Neuroreport. 2017 May 24;28(8):444-450.

Additional Infomation
Dizocilpine maleate is a maleate salt obtained by reaction of dizocilpine with one equivalent of maleic acid. It has a role as an anaesthetic, an anticonvulsant, a neuroprotective agent, a nicotinic antagonist and a NMDA receptor antagonist. It is a maleate salt and a tetracyclic antidepressant. It contains a dizocilpine(1+).
A potent noncompetitive antagonist of the NMDA receptor (RECEPTORS, N-METHYL-D-ASPARTATE) used mainly as a research tool. The drug has been considered for the wide variety of neurodegenerative conditions or disorders in which NMDA receptors may play an important role. Its use has been primarily limited to animal and tissue experiments because of its psychotropic effects.
The compound MK-801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d] cyclohepten-5,10-imine maleate)] is a potent anticonvulsant that is active after oral administration and whose mechanism of action is unknown. We have detected high-affinity (Kd = 37.2 +/- 2.7 nM) binding sites for [3H]MK-801 in rat brain membranes. These sites are heat-labile, stereoselective, and regionally specific, with the hippocampus showing the highest density of sites, followed by cerebral cortex, corpus striatum, and medulla-pons. There was no detectable binding in the cerebellum. MK-801 binding sites exhibited a novel pharmacological profile, since none of the major neurotransmitter candidates were active at these sites. The only compounds that were able to compete for [3H]MK-801 binding sites were substances known to block the responses of excitatory amino acids mediated by the N-methyl-D-aspartate (N-Me-D-Asp) receptor subtype. These comprised the dissociative anesthetics phencyclidine and ketamine and the sigma-type opioid N-allylnormetazocine (SKF 10,047). Neurophysiological studies in vitro, using a rat cortical-slice preparation, demonstrated a potent, selective, and noncompetitive antagonistic action of MK-801 on depolarizing responses to N-Me-D-Asp but not to kainate or quisqualate. The potencies of phencyclidine, ketamine, SKF 10,047, and the enantiomers of MK-801 as N-Me-D-Asp antagonists correlated closely (r = 0.99) with their potencies as inhibitors of [3H]MK-801 binding. This suggests that the MK-801 binding sites are associated with N-Me-D-Asp receptors and provides an explanation for the mechanism of action of MK-801 as an anticonvulsant.[1]
Whole-cell and single-channel recording techniques were used to study the action of the anticonvulsant drug MK-801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]- cyclohepten-5,10-imine maleate) on responses to excitatory amino acids in rat neocortical neurons in cell culture. MK-801 caused a progressive, long-lasting blockade of current induced by N-methyl-D-aspartate (N-Me-D-Asp). However, during the time that N-Me-D-Asp responses were inhibited, there was no effect on responses to quisqualate or kainate, suggesting that N-Me-D-Asp receptors and kainate/quisqualate receptors open separate populations of ion channels. Binding and unbinding of MK-801 seems to be possible only if the N-Me-D-Asp-operated channel is in the transmitter-activated state: MK-801 was effective only when applied simultaneously with N-Me-D-Asp, and recovery from MK-801 blockade was speeded by continuous exposure to N-Me-D-Asp [time constant (tau) approximately equal to 90 min at -70 to -80 mV]. Recovery from block during continuous application of N-Me-D-Asp was strongly voltage dependent, being faster at positive potentials (tau approximately equal to 2 min at +30 mV). Mg2+, which is thought to block the N-Me-D-Asp-activated ion channel, inhibited blockade by MK-801 at negative membrane potentials. In single-channel recordings from outside-out patches. MK-801 greatly reduced the channel activity elicited by application of N-Me-D-Asp but did not significantly alter the predominant unitary conductance. Consistent with an open-channel blocking mechanism, the mean channel open time was reduced by MK-801 in a dose-dependent manner.[3]
In summary, our work shows for the first time that the same reactivation parameters and pharmacological agent (MK-801) that disrupted the reconsolidation of a cocaine-associated memory for a CPP task did not disrupt reconsolidation of the memory for a self-administration task. Further, reactivation parameters that mimicked the self-administration procedure itself, and therefore should have promoted robust retrieval of the cocaine-associated memory, also failed to render this memory labile for disruption by MK-801. The possibility of diminishing persistent and unwanted memories by disrupting the reconsolidation process opens exciting new frontiers for developing treatments for pathological disorders, including drug abuse. However, the complexity of memory storage and subsequent memory retrieval that ultimately may lead to memory recoding has only begun to be elucidated and therefore requires further systematic investigation with regard to the timing and the specific parameters used for reactivation.[5]
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C20H19NO4
Molecular Weight
337.3692
Exact Mass
337.131
Elemental Analysis
C, 71.20; H, 5.68; N, 4.15; O, 18.97
CAS #
77086-22-7
Related CAS #
(-)-Dizocilpine maleate;121917-57-5;Dizocilpine;77086-21-6
PubChem CID
6420042
Appearance
White to off-white solid powder
Boiling Point
541ºC at 760 mmHg
Melting Point
183-185ºC
Flash Point
281ºC
LogP
3.19
Hydrogen Bond Donor Count
3
Hydrogen Bond Acceptor Count
5
Rotatable Bond Count
2
Heavy Atom Count
25
Complexity
432
Defined Atom Stereocenter Count
2
SMILES
C[C@@]12C3=CC=CC=C3C[C@@H](N1)C4=CC=CC=C24.C(=C\C(=O)O)\C(=O)O
InChi Key
QLTXKCWMEZIHBJ-BTJKTKAUSA-N
InChi Code
InChI=1S/C16H15N.C4H4O4/c1-16-13-8-4-2-6-11(13)10-15(17-16)12-7-3-5-9-14(12)16;5-3(6)1-2-4(7)8/h2-9,15,17H,10H2,1H3;1-2H,(H,5,6)(H,7,8)/b;2-1-
Chemical Name
5-methyl-10,11-dihydro-5H-5,10-epiminodibenzo[a,d][7]annulene maleate
Synonyms
Dizocilpine;MK801; MK 801; MK-801;DIZOCILPINE MALEATE; (+)-MK-801 hydrogen maleate; Dizocilpine maleate [USAN]; 6LR8C1B66Q; DTXSID2045785; DIZOCILPINE MALEATE; 77086-22-7; (+)-MK 801 Maleate; (+)-MK-801 hydrogen maleate; Dizocilpine hydrogen maleate; Dizocilpine maleate [USAN]; UNII-6LR8C1B66Q; 6LR8C1B66Q; (+)-MK 801 hydrogen maleate; MK 801 Maleate
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.
Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO: 68 mg/mL (201.6 mM)
Water:<1 mg/mL
Ethanol:<1 mg/mL
Solubility (In Vivo)
Solubility in Formulation 1: ≥ 2.5 mg/mL (7.41 mM) (saturation unknown) in 10% EtOH + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear EtOH stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

Solubility in Formulation 2: ≥ 2.5 mg/mL (7.41 mM) (saturation unknown) in 10% EtOH + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear EtOH stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.19 mg/mL (6.49 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 21.9 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.


Solubility in Formulation 4: ≥ 2.08 mg/mL (6.17 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

Solubility in Formulation 5: ≥ 2.08 mg/mL (6.17 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

Solubility in Formulation 6: 3.45 mg/mL (10.23 mM) in Saline (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 2.9641 mL 14.8205 mL 29.6410 mL
5 mM 0.5928 mL 2.9641 mL 5.9282 mL
10 mM 0.2964 mL 1.4821 mL 2.9641 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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Molarity Calculator allows you to calculate the mass, volume, and/or concentration required for a solution, as detailed below:

  • Calculate the Mass of a compound required to prepare a solution of known volume and concentration
  • Calculate the Volume of solution required to dissolve a compound of known mass to a desired concentration
  • Calculate the Concentration of a solution resulting from a known mass of compound in a specific volume
An example of molarity calculation using the molarity calculator is shown below:
What is the mass of compound required to make a 10 mM stock solution in 5 ml of DMSO given that the molecular weight of the compound is 350.26 g/mol?
  • Enter 350.26 in the Molecular Weight (MW) box
  • Enter 10 in the Concentration box and choose the correct unit (mM)
  • Enter 5 in the Volume box and choose the correct unit (mL)
  • Click the “Calculate” button
  • The answer of 17.513 mg appears in the Mass box. In a similar way, you may calculate the volume and concentration.

Dilution Calculator allows you to calculate how to dilute a stock solution of known concentrations. For example, you may Enter C1, C2 & V2 to calculate V1, as detailed below:

What volume of a given 10 mM stock solution is required to make 25 ml of a 25 μM solution?
Using the equation C1V1 = C2V2, where C1=10 mM, C2=25 μM, V2=25 ml and V1 is the unknown:
  • Enter 10 into the Concentration (Start) box and choose the correct unit (mM)
  • Enter 25 into the Concentration (End) box and select the correct unit (mM)
  • Enter 25 into the Volume (End) box and choose the correct unit (mL)
  • Click the “Calculate” button
  • The answer of 62.5 μL (0.1 ml) appears in the Volume (Start) box
g/mol

Molecular Weight Calculator allows you to calculate the molar mass and elemental composition of a compound, as detailed below:

Note: Chemical formula is case sensitive: C12H18N3O4  c12h18n3o4
Instructions to calculate molar mass (molecular weight) of a chemical compound:
  • To calculate molar mass of a chemical compound, please enter the chemical/molecular formula and click the “Calculate’ button.
Definitions of molecular mass, molecular weight, molar mass and molar weight:
  • Molecular mass (or molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
  • Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.
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Reconstitution Calculator allows you to calculate the volume of solvent required to reconstitute your vial.

  • Enter the mass of the reagent and the desired reconstitution concentration as well as the correct units
  • Click the “Calculate” button
  • The answer appears in the Volume (to add to vial) box
In vivo Formulation Calculator (Clear solution)
Step 1: Enter information below (Recommended: An additional animal to make allowance for loss during the experiment)
Step 2: Enter in vivo formulation (This is only a calculator, not the exact formulation for a specific product. Please contact us first if there is no in vivo formulation in the solubility section.)
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Calculation results

Working concentration mg/mL;

Method for preparing DMSO stock solution mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.

Method for preparing in vivo formulation:Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.

(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
             (2) Be sure to add the solvent(s) in order.

Biological Data
  • An external file that holds a picture, illustration, etc. Object name is nihms71896f4.jpg
    Differential MK-801 block and recovery of NMDA-eEPSCs and NMDA-mEPSCs.

  • An external file that holds a picture, illustration, etc. Object name is nihms71896f1.jpg
    MK-801 block of NMDA-mEPSCs in hippocampal cultures.


  • An external file that holds a picture, illustration, etc. Object name is nihms71896f9.jpg
    Asynchronous release detected in the absence of synaptotagmin 1 or in strontium is resistant to MK-801 application at rest.
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