> Chemicals & Drugs > Organic Chemical > WIN 55,212

← WILD 20

Wogonin →

WIN 55,212

WIN 55,212 is a synthetic cannabinoid receptor agonist with potent analgesic, anti-inflammatory, and neuroprotective effects.
It acts primarily on the CB1 and CB2 receptors, modulating endocannabinoid signaling pathways.
WIN 55,212 has demonstrated efficacy in preclinical models of pain, neurological disorders, and other conditions, making it a subject of ongoing research and development.
Its potential therapeutic applications and pharmacological profile continue to be explored by scientists and clinicians.

Most cited protocols related to «WIN 55,212»

Cannabinoid Receptor Binding Assay

Cited 4 times

Protocol full text hidden due to copyright restrictions

Open the protocol to access the free full text link

Publication 2012

Brain Buffers Cannabinoids Cold Temperature CP-55,940 Ethanol Filtration Magnesium Chloride Mice, House Radioactivity Serum Albumin, Bovine Spectrophotometry Tromethamine Vacuum WIN 55,212

Radioligand Binding Assay for CB1 Receptors

Cited 4 times

Fifty µg of mouse brain membrane homogenates (containing a relatively pure source of CB1Rs) were incubated with 0.2 nM of the radiolabeled cannabinoid agonist [³H]CP-55,940 for 90 min at room temperature in an assay buffer containing 5 mM MgCl₂, 50 mM Tris, 0.05% bovine serum albumin (BSA) and increasing concentrations (0.1 nM–10 µM) of JWH-018 M1–M6, or non-radioactive CP-55,940. Assays were performed in triplicate, in a final volume of 1 mL, as previously described [59] (link). Total binding was defined as the amount of radioactivity observed when 0.2 nM [³H]CP-55,940 was incubated in the absence of any competitor. Nonspecific binding was defined as the amount of [³H]CP-55,940 binding remaining in the presence of 10 µM of the non-radioactive CB1/CB2 cannabinoid agonist WIN-55,212-2. Specific binding was calculated by subtracting non-specific from total binding. Reactions were terminated by quick filtration through Whatman GF/B glass fiber filters, followed by five washes with an ice-cold buffer containing 50 mM Tris and 0.05% bovine serum albumin (BSA). Filters were punched out into 7 mL scintillation vials and immersed in 4 mL of ScintiVerse™ BD Cocktail scintillation fluid. After overnight extraction, bound radioactivity was determined by liquid scintillation spectrophotometry. Specific binding is expressed as a percentage of binding occurring in vehicle samples (e.g., binding in the absence of any competitor).

Brents L.K., Reichard E.E., Zimmerman S.M., Moran J.H., Fantegrossi W.E, & Prather P.L. (2011). Phase I Hydroxylated Metabolites of the K2 Synthetic Cannabinoid JWH-018 Retain In Vitro and In Vivo Cannabinoid 1 Receptor Affinity and Activity. PLoS ONE, 6(7), e21917.

Full text: Click here

Publication 2011

Biological Assay Brain Buffers Cannabinoid Receptor Agonists Cold Temperature CP-55,940 Exhaling Filtration JWH 018 Magnesium Chloride Mice, House Radioactivity Serum Albumin, Bovine Spectrophotometry Tissue, Membrane Tromethamine WIN 55,212

Repeated Water Avoidance Stress in Rats

Cited 4 times

Repeated water avoidance (WA) stress to adult rats was conducted as described previously.^{12 (link)} The rats were placed on the glass platform in the middle of a test Plexiglas tank that was filled with water (25°C) to 1 cm below the height of the platform. The animals were maintained on the block for 1 hour daily for 10 consecutive days. This repeated WA procedure represents a potent psychological stressor.^{13 (link)} The sham control rats were placed similarly for 1 hour daily for 10 days in the container without water. In a separate study, a group of 8 rats were subcutaneously injected with WIN (2 mg/kg) consecutively for 10 days after rats were subjected to WA stress. A group of 9 WA stress rats were injected IP with capsazepine (5 mg/kg) one hour before the VMR assessment. WIN 55,212-2 and capsazepine were dissolved in 10% DMSO/5% Tween 80/85% saline and the doses were selected based on published reports.^{14 (link), 15 (link)}

Hong S., Fan J., Kemmerer E.S., Evans S., Li Y, & Wiley J.W. (2008). Reciprocal Changes in Vanilloid (TRPV1) and Endocannabinoid (CB1) Receptors Contribute to Visceral Hyperalgesia in the Water Avoidance Stressed Rat. Gut, 58(2), 202-210.

Publication 2008

Adult Animals capsazepine Plexiglas Rattus norvegicus Saline Solution Stress, Psychological Sulfoxide, Dimethyl Tween 80 Tween 85 Water Stress WIN 55,212

Cannabinoid Receptor Binding Assays

Cited 4 times

Protocol full text hidden due to copyright restrictions

Open the protocol to access the free full text link

Publication 2008

Biological Assay Buffers Cardiac Arrest Cells Cold Temperature CP-55,940 Edetic Acid Filtration Ligands Magnesium Chloride Membrane Proteins Pellets, Drug prisma Proteins Radioactivity Scintillation Counters Strains Tissue, Membrane Tromethamine Ultracentrifugation WIN 55,212

Electrophysiological Characterization of Lateral Habenula Neurons

Cited 3 times

Whole cell and cell-attached recordings were performed on LHb slices using a patch amplifier (Multiclamp 700B) under infrared-differential interference contrast microscopy. Data acquisition and analysis were carried out using DigiData 1440A, pClamp 10 (molecular devices, Union City, CA), Clampfit and Mini Analysis 6.0.3 (Synaptosoft Inc.). Signals were filtered at 3 kHz and digitized at 10 kHz. The recording ACSF was the same as the cutting solution except that it was ascorbic acid-free. Spontaneous activity was monitored using cell-attached voltage-clamp recordings of action potentials (APs) at I = 0 pA for 5 minutes. Number of APs was counted over 5 min and spike frequency was calculated. Neuronal excitability recordings in response to depolarization were performed in whole-cell current-clamp mode. The patch pipettes (3–6 MΩ) were filled with 130 mM K-gluconate, 15 mM KCl, 4 mM ATP-Na+, 0.3 mM GTP-Na+, 1 mM EGTA, and 5 mM HEPES (pH adjusted to 7.28 with KOH, osmolarity adjusted to 275–280 mOsm). LHb neurons were given increasingly depolarizing current steps at +10pA intervals ranging from +10pA to +100pA, allowing us to measure AP generation in response to membrane depolarization (5 sec duration). Current injections were separated by a 20s interstimulus interval and neurons were kept at −65 mV with manual direct current injection between pulses. Synaptic transmission blockade was achieved by adding 6,7-dinitroquinoxaline-2,3-dione (DNQX; 10 µM), picrotoxin (100µM) and APV (50 µM) to block AMPA, GABA_A and NMDA receptor-mediated synaptic transmission, respectively. The number of APs induced by depolarization at each intensity was counted and averaged for each experimental group.
Because AHP amplitude increases with increasing number of APs, we measured AP threshold, mAHP and fAHP amplitudes at the current step that was sufficient to generate the first AP/s (58 (link)). AP threshold was measured at the beginning of the upward rise of the AP. mAHP was measured as the difference between AP threshold and the peak negative membrane potential at the end of the current step. fAHPs were calculated as the difference between AP threshold and the peak negative potential following the AP (Figure 1E). Resting membrane potential (RMP) was assessed at the beginning of the recording by quickly switching to I=0. Input resistance (Rin) was determined by injecting a small (50 pA) hyperpolarizing current pulse (5s) and calculated by dividing the steady-state voltage response by the current pulse amplitude. Reported AP half width, AP peak amplitude were obtained from measurements of AP characteristics in Clampfit.
Whole-cell recordings of GABA_AR-mediated mIPSCs were isolated in ACSF perfused with DNQX; 10 µM, strychnine (1 µM) and tetrodotoxin (TTX, 1 µM). The patch pipettes (3–6 MΩ) were filled with 125 mM KCl, 2.8 mM NaCl, 2 mM MgCl₂, 2 mM ATP-Na⁺, 0.3 mM GTP-Na⁺, 0.6 mM EGTA, and 10 mM HEPES (pH adjusted to 7.28 with KOH, osmolarity adjusted to 275–280 mOsm). AMPAR-mediated mEPSCs were isolated in ACSF perfused with picrotoxin (100µM), D-APV (50µM) and TTX (1 µM). Patch pipettes for mEPSC recordings were filled with 117 mM Cs-gluconate, 2.8 mM NaCl, 5 mM MgCl₂, 2 mM ATP-Na⁺, 0.3 mM GTP-Na⁺, 0.6 mM EGTA, and 20 mM HEPES (pH adjusted to 7.28 with CsOH, osmolarity adjusted to 275–280 mOsm). For both mIPSCs and mEPSCs, LHb neurons were voltage-clamped at −70 mV and recorded over 10 sweeps, each lasting 50 seconds.
EPSCs were evoked with a stimulating electrode placed in the stria medullaris. Evoked EPSCs were recorded in ACSF perfusion containing picrotoxin (100µM) while the cell was voltage-clamped at +40 mV. Internal solution for patch pipettes was similar to that used for mEPSC recordings (Cs-gluconate-based) but also included intracellular spermine (10µM). AMPAR-mediated currents were isolated with D-APV (50 µM), a selective NMDA receptor antagonist. Isolated AMPAR-mediated currents were then subtracted from the combined EPSC to provide the NMDA receptor-mediated current and thus, the AMPA/NMDA ratio. AMPAR EPSCs were also recorded at holding potentials ranging from −65 to +40 mV in the presence of picrotoxin (100µM), APV (50 µM) and intracellular spermine (10 µM) included in Cs-gluconate-based internal. Normalized current-voltage (I–V) curves were then generated by dividing the AMPAR EPSC peak amplitudes by the mean of AMPAR EPSC peak amplitude recorded at −65 mV. AMPAR EPSC rectification was determined by dividing peak AMPAR EPSCs amplitudes recorded at −65 mV by those recorded at +40 mV.
The excitatory and inhibitory balance (EPSC/IPSC, E/I ratio,) was recorded with a Cs-gluconate-based internal solution similar to mEPSC recordings. Evoked EPSCs and IPSCs from LHb neurons were recorded in the same neuron in drug-free ASCF using a stimulating electrode placed in the stria medullaris. EPSCs were recorded at the reversal potential for GABA_A IPSCs (−55 mV), and IPSCs were recorded at the reversal potential for EPSCs (+10 mV) in the same LHb neuron. The E/I ratio was then calculated as EPSC/IPSC amplitude ratio by dividing the average peak amplitude of 10 consecutive sweeps of EPSCs or IPSCs from the same recording. The cell input resistance and series resistance were monitored through all the experiments and if these values changed by more than 10%, data were not included.
Antalarmin, CYPPA, 1-EBIO, WIN 55,212-2 and AM251 were prepared as stock solution in DMSO and were diluted (1:10000) to final concentration in ACSF of 1µM, 10µM, 300mM, 2µM, and 10µM, respectively. Stock solutions for apamin, rat CRF, iberiotoxin, and Antisauvagine-30 were prepared in distilled water and diluted (1:1000) to final concentration in ACSF of 100nM, 250nM, 100nM, and 25nM, respectively. The intra-pipette concentrations of BAPTA, GDPβs and PKI(6–22) were 30mM, 300µM, and 10µM, respectively. In some of our control interleaved experiments, AP recordings were continued for an hour without addition of drugs and no significant changes were observed over time. For all drug experiments, a baseline depolarization-induced AP recording/ mIPSC/mEPSC was recorded in each neuron, and then the appropriate drug was added to the slice by the perfusate and AP generation in response to depolarizing current steps was again tested 25–30 min after. For apamin and CYPPA experiments, a second baseline with apamin or CYPPA was obtained before the addition of CRF and AP generation was re-evaluated 25–30min after CRF application. CRF wash-out experiments in Supplementary figures were performed following 15min of bath application of CRF and the recordings continued at least for 90 min after the initiation of wash out of CRF.

Authement M.E., Langlois L.D., Shepard R.D., Browne C.A., Lucki I., Kassis H, & Nugent F.S. (2018). A role for corticotrophin releasing factor signaling in the lateral habenula and its modulation by early life stress. Science signaling, 11(520), eaan6480.

Publication 2018

1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid 1-ethyl-2-benzimidazolinone 6,7-dinitroquinoxaline-2,3-dione Action Potentials alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid AM 251 antalarmin antisauvagine 30 Apamin Ascorbic Acid Bath Cardiac Arrest Cells Egtazic Acid gluconate guanosine 5'-O-(2-thiodiphosphate) HEPES iberiotoxin Induced Pluripotent Stem Cells K 130 Magnesium Chloride Medical Devices Membrane Potentials Microscopy, Differential Interference Contrast N-Methyl-D-Aspartate Receptors N-Methylaspartate Neurons Osmolarity Perfusion Pharmaceutical Preparations Picrotoxin Protoplasm Psychological Inhibition Pulse Rate Pulses Sodium Chloride Spermine Striae Distensae Strychnine Sulfoxide, Dimethyl Synaptic Transmission Tissue, Membrane WIN 55,212

Most recents protocols related to «WIN 55,212»

Binding Assay for Human CB2 Receptor

The compounds selected
for the in vitro binding assay were purchased via MolPort, SIA, Riga,
Latvia (Supporting Information S2). Membrane
preparations from CHO-K1 cells expressing the human CB2 (ChemiSCREEN
Membrane Preparation Recombinant Human CB2 Cannabinoid Receptor. Merck,
USA) were incubated in duplicate with 0.8 nM [³H]CP-55,940
(specific activity: 101 Ci/mmole, PerkinElmer, USA) in a 50 mM Tris–HCl,
pH = 7.4 buffer supplemented with 2.5 mM EDTA, 5 mM MgCl₂, 0.5 mg/mL BSA and increasing concentrations of the compounds tested.
Compounds were dissolved in 50% DMSO and added to the reaction mixture
at 10 concentrations equally spaced on a log scale (10^–10–10^–4.5 M). The final DMSO concentration
was 5%. Nonspecific binding was determined with 10 μM WIN 55,212-2.
The reaction mixture (500 μL) was incubated for 1.5 h at 30
°C. Before harvesting, Brandel Whatman GF/B Filter Paper was
presoaked with 0.5% polyethylenimine buffer for 30 min and then washed
with 2 mL of 50 mM Tris–HCl buffer (pH = 7.4) containing 0.5%
BSA to minimize nonspecific binding. The reaction was terminated by
depositing the samples onto the filter paper with the Brandel M–24
Cell Harvester. Samples were then rapidly washed three times with
2 mL of wash buffer (50 mM Tris–HCl pH 7.4, 2.5 mM EDTA, 5
mM MgCl₂, 0.5 mg/mL BSA) to separate the bound radioligand
from free. Filters were then air-dried for 1.5 h at 60 °C. After
drying, filter discs were placed on a flexible 24-well plate and 500
μL of EcoScint-20 scintillant (PerkinElmer, USA) was added to
each well. Plates were counted (2 min per well) in a Trilux MicroBeta
counter (PerkinElmer, USA). Data were analyzed with GraphPad Prism
5.0 software. Curves were fitted with a one-site nonlinear regression
model, and inhibitory constants (pK_i ±
SEM and K_i, 95% CI) were calculated from
the Cheng–Prusoff equation.

Stasiulewicz A., Lesniak A., Bujalska-Zadrożny M., Pawiński T, & Sulkowska J.I. (2023). Identification of Novel CB2 Ligands through Virtual Screening and In Vitro Evaluation. Journal of Chemical Information and Modeling, 63(3), 1012-1027.

Full text: Click here

Publication 2023

Biological Assay Buffers CHO Cells CP-55,940 Edetic Acid Homo sapiens Magnesium Chloride Polyethyleneimine Psychological Inhibition Receptor, Cannabinoid Sulfoxide, Dimethyl Tromethamine WIN 55,212

CB2R Agonist Ligand Docking and Optimization

All ligands are built and optimized using Maestro, considering for JR compounds both cis- conformers of the 4-methyl cyclohexyl group; they were subjected to a Conformational Search (CS) of 1000 steps in a water environment using the Macromodel program. The Monte Carlo algorithm was used with the MMFFs forcefield. The ligands were then minimized using the Conjugated Gradient method to a convergence value of 0.05 kcal/Å∙mol using the same forcefield and parameters as for the CS. The central scaffold of compounds JR22 and JR64, the N-(4-methylcyclohexyl)-2-oxo-1,2-dihydro-1,8-naphthyridine-3-carboxamide was built, and both cis-conformers (bearing the amide moiety in an axial or equatorial position) were subjected to a B3LYP/6-31G** optimization, in order to evaluate the best conformer. Crystallographic structures 6PT0 [17 (link)], relative to the active conformation of CB2R, already refined through Maestro, had been used for docking LV62, EC21a, CP55,940, and all JR compounds using the GOLD program, applying the same procedure described in our previous study on 2-oxo-pyridine derivatives. For docking LV62, the region of interest was defined in such a manner that the protein contained all the residues within 10 Å of WIN 55,212-2. All JR compounds were subjected to docking in the empty orthosteric cavity, with a scaffold constraint of strength 5 on the LV62 core of the docked pose; in this way, the orthosteric pharmacophoric portion of JR compounds can fit the usual CB2R agonist cavity, whereas the EC21a-derived allosteric tail can be free to reach a favorable binding site. In the same condition, also the free calculation, without any scaffold constraint, was performed. The “allow early termination” command was always deactivated. All ligands were submitted to 40 Genetic Algorithm runs using Chemscore, ASP, PLP, and Goldscore fitness functions, clustering the output orientations on the basis of an RMSD distance of 1.5 Å. The default GOLD parameters were used for all other variables. Docking results were analyzed by using Chimera 1.16.

Ferrisi R., Polini B., Ricardi C., Gado F., Mohamed K.A., Baron G., Faiella S., Poli G., Rapposelli S., Saccomanni G., Aldini G., Chiellini G., Laprairie R.B., Manera C, & Ortore G. (2023). New Insights into Bitopic Orthosteric/Allosteric Ligands of Cannabinoid Receptor Type 2. International Journal of Molecular Sciences, 24(3), 2135.

Full text: Click here

Publication 2023

Amides Binding Sites Birth Chimera Crystallography Dental Caries derivatives Gold Ligands Mental Orientation methyl 2-O-methylfucofuranoside Proteins pyridine Tail WIN 55,212

Receptor Interaction Signature Analysis

To
systematically compare the LRIPs, we summarized the ligand–residue
interaction energies for the CB1/CB2 active/inactive systems. To achieve
this, we first selected known active compounds for each receptor according
to the MM-PBSA binding free energies. In detail, AM-4030, AM-11542,
THC, and WIN-55,212–2 were selected for active CB1; THC, AM-4030,
WIN-55,212–2, and UR-144 were selected for active CB2; SR-147778,
AM-251, MK-0364, and THC were selected for inactive CB1; AM-10257,
AM-630, and THC were selected for inactive CB2. Then, we selected
the key residues for each protein–ligand system if the ligand–residue
interaction energies are stronger than −0.1 kcal/mol. Next,
we calculated the average of these ligand–residue interaction
energies for key residues. The mean IPs can be considered a signature
of a receptor in an active or inactive form. At last, for a given
compound in question, its IP similarity to the receptor IP signature
was evaluated using four metrics, average standard error (ASE), root-mean-square
deviation (RMSE), average unsigned error (AUE), and squared correlation
coefficient (R²).
In this work,
we are more interested in designing agonists. Thus, we first evaluated
whether a query compound is an agonist in priority. If the R between
a compound and selected known agonists is higher than 0.84 (R² > 0.7) and meanwhile, the binding energy
(ΔE) is better than −10 kcal/mol, then,
it is considered
to be a potential agonist. Otherwise, we determine that the compound
is probably an antagonist or an undetermined compound (Figure 2).

Ge H., Ji B., Fang J., Wang J., Li J, & Wang J. (2023). Discovery of Potent and Selective CB2 Agonists Utilizing a Function-Based Computational Screening Protocol. ACS Chemical Neuroscience, 14(21), 3941-3958.

Full text: Click here

Publication 2023

agonists Ligands MK 0364 Plant Roots poly(tetramethylene succinate-co-tetramethylene adipate) Proteins SR 147778 UR-144 WIN 55,212

Radioligand Binding Assay for hCB1R and hCB2R

The binding affinities toward
hCB1R and hCB2R were determined according
to a previously published protocol.²² In
brief, membrane preparations obtained from CHO cell lines stably transfected
with either human CB1R (hCB1R-CHO; obtained from Euroscreen, Gosselies,
Belgium) or human CB2R (hCB2R-CHO; obtained from Paul L. Prather,
Department of Pharmacology and Toxicology, College of Medicine, University
of Arkansas for Medical Sciences, USA) were incubated with [³H]SR141716A (1,554 GBq/mmol; PerkinElmer Life and Analytical Sciences,
Rodgau, Germany; final concentration ∼2 nM) or [³H]WIN55212-2 (6,438 GBq/mmol; PerkinElmer Life and Analytical Sciences,
Rodgau, Germany; final concentration ∼3 nM) and the respective
test compounds at different concentrations (final concentration 10^–5–10^–11 M) diluted from DMSO
stock solutions (1% DMSO final concentration) in incubation buffer
(50 mM TRIS-HCl, pH 7.4, supplemented with 0.1% bovine serum albumin,
5 mM MgCl₂, and 1 mM EDTA) at rt for 90 min.
Homologous
radioligand displacement studies investigating the potential of RM365
to displace [¹⁸F]RM365 from binding sites in membrane homogenates
of rat spleen or hCB2R-CHO cells were performed according to the same
protocol.
The nonspecific binding of the respective radioligand
was determined
by coincubation with CP55,940 (final concentration 10^–5 M). The normalized values of bound activity (% specific binding)
were calculated and plotted vs the logarithm of the concentration
of the respective test compound. The IC₅₀ values of the
resulting inhibition curves were estimated by nonlinear regression
analysis (GraphPad Prism 2.01). To calculate the K_i, the equation of Cheng and Prusoff was used. For homologous
competition experiments, K_i = K_D.^{38 (link)}

Teodoro R., Gündel D., Deuther-Conrad W., Kazimir A., Toussaint M., Wenzel B., Bormans G., Hey-Hawkins E., Kopka K., Brust P, & Moldovan R.P. (2023). Synthesis, Structure–Activity Relationships, Radiofluorination, and Biological Evaluation of [18F]RM365, a Novel Radioligand for Imaging the Human Cannabinoid Receptor Type 2 (CB2R) in the Brain with PET. Journal of Medicinal Chemistry, 66(20), 13991-14010.

Full text: Click here

Publication 2023

Binding Sites Buffers Cell Lines CHO Cells Edetic Acid Homo sapiens Magnesium Chloride Pharmaceutical Preparations prisma Psychological Inhibition Serum Albumin, Bovine Spleen SR 141716A Sulfoxide, Dimethyl Tissue, Membrane Tromethamine WIN 55,212

Chondrocyte Expansion and Characterization

Win 55,212-2 mesylate salt ≥98% (Sigma-Aldrich, St. Louis, MO, USA), dimethyl sulfoxide (DMSO, Life Technologies, Carlsbad, CA, USA), transforming growth factor-β3 (Peprotech, Rocky Hill, NJ, USA), insulin-transferrin-selenium supplement (Invitrogen), antibiotic-antimycotic (Invitrogen), Quant-iT PicoGreen dsDNA reagent and kits (Invitrogen), TRIZOL reagent (Invitrogen), SuperScript VILO cDNA synthesis kit (Invitrogen), Applied Biosystems Power SYBR Green PCR Master Mix (Invitrogen), and 10% buffered formalin phosphate solution (Fisher Chemical, Fair Lawn, NJ, USA) were used. CellTiter 96 AQueous One Solution cell proliferation assay (MTS) and Accumax cell dissociation solution were purchased from Promega (Madison, WI, USA) and Innovative Cell Technologies (San Diego, CA, USA), respectively.

Shang J., Hines S., Makarczyk M.J., Lin H., Hogan M.V, & Yan A. (2023). Influence of the Synthetic Cannabinoid Agonist on Normal and Inflamed Cartilage: An In Vitro Study. Biomolecules, 13(10), 1502.

Full text: Click here

Publication 2023

Anabolism Antibiotics Biological Assay Cell Proliferation Cells Dietary Supplements DNA, Complementary DNA, Double-Stranded Formalin Insulin Mesylates Phosphates PicoGreen Promega Selenium Sodium Chloride Sulfoxide, Dimethyl SYBR Green I Transferrin Transforming Growth Factors trizol WIN 55,212

Top products related to «WIN 55,212»

Win55 212 2 by Bio-Techne

Sourced in United Kingdom, United States

WIN55,212-2 is a synthetic cannabinoid receptor agonist. It binds to and activates both CB1 and CB2 cannabinoid receptors. This product is intended for laboratory research use only.

Win 55 212 2 by Merck Group

Sourced in United States, Germany, Spain, Sao Tome and Principe

WIN 55,212-2 is a synthetic cannabinoid compound that has been used in research and laboratory settings. It acts as an agonist at cannabinoid receptors. The compound has been utilized in various experimental studies, but a detailed description of its core function without extrapolation on intended use cannot be provided while maintaining an unbiased and factual approach.

Win55 212 2 by Cayman Chemical

Sourced in United States

WIN55,212-2 is a synthetic chemical compound that acts as a cannabinoid receptor agonist. It is commonly used in scientific research as a tool compound to study the endocannabinoid system.

Am251 by Bio-Techne

Sourced in United Kingdom, United States, Italy, France

AM251 is a synthetic cannabinoid receptor antagonist. It functions by selectively binding to and inhibiting the CB1 cannabinoid receptor.

Dimethyl sulfoxide (dmso) by Merck Group

Sourced in United States, Germany, United Kingdom, China, Italy, Sao Tome and Principe, France, Macao, India, Canada, Switzerland, Japan, Australia, Spain, Poland, Belgium, Brazil, Czechia, Portugal, Austria, Denmark, Israel, Sweden, Ireland, Hungary, Mexico, Netherlands, Singapore, Indonesia, Slovakia, Cameroon, Norway, Thailand, Chile, Finland, Malaysia, Latvia, New Zealand, Hong Kong, Pakistan, Uruguay, Bangladesh

DMSO is a versatile organic solvent commonly used in laboratory settings. It has a high boiling point, low viscosity, and the ability to dissolve a wide range of polar and non-polar compounds. DMSO's core function is as a solvent, allowing for the effective dissolution and handling of various chemical substances during research and experimentation.

Tween 80 by Merck Group

Sourced in United States, Germany, United Kingdom, India, Italy, France, Sao Tome and Principe, Spain, Poland, China, Belgium, Brazil, Switzerland, Canada, Australia, Macao, Ireland, Chile, Pakistan, Japan, Denmark, Malaysia, Indonesia, Israel, Saudi Arabia, Thailand, Bangladesh, Croatia, Mexico, Portugal, Austria, Puerto Rico, Czechia

Tween 80 is a non-ionic surfactant and emulsifier. It is a viscous, yellow liquid that is commonly used in laboratory settings to solubilize and stabilize various compounds and formulations.

Cp55 940 by Bio-Techne

Sourced in United Kingdom, United States

CP55,940 is a high-affinity cannabinoid receptor agonist. It binds to both CB1 and CB2 receptors with high potency.

Damgo by Bio-Techne

Sourced in United Kingdom, United States

DAMGO is a synthetic opioid peptide that acts as a selective agonist for the mu-opioid receptor. It is commonly used in research applications to study the pharmacology and function of the mu-opioid receptor.

Win 55 212 2 mesylate by Bio-Techne

Sourced in United States, United Kingdom

WIN 55,212-2 mesylate is a synthetic cannabinoid receptor agonist. It primarily binds to and activates the CB1 and CB2 cannabinoid receptors. WIN 55,212-2 mesylate is commonly used as a research tool in the study of the endocannabinoid system.

Am251 by Merck Group

Sourced in United States, Germany, Italy

AM251 is a chemical compound used in laboratory research settings. It functions as an antagonist for the CB1 cannabinoid receptor. This means it binds to and blocks the activity of this specific receptor, which is involved in various physiological processes. The core purpose of AM251 is to facilitate the study of the CB1 receptor and its role in different biological systems.

What is the chemical structure and primary pharmacology of WIN 55,212?

WIN 55,212 is a synthetic cannabinoid receptor agonist that acts primarily on the CB1 and CB2 receptors. It has a unique chemical structure that allows it to modulate endocannabinoid signaling pathways, leading to potent analgesic, anti-inflammatory, and neuroprotective effects. Understanding the specifics of WIN 55,212's pharmacological profile is crucial for optimizing its use in research and potential therapeutic applications.

What are some of the key therapeutic applications of WIN 55,212 that have been explored in preclinical research?

Preclinical studies have demonstrated the efficacy of WIN 55,212 in various animal models of pain, neurological disorders, and other conditions. For example, it has shown promise in alleviating neuropathic pain, reducing inflammation, and providing neuroprotection in models of neurodegenerative diseases. Researchers continue to investigate the potential of WIN 55,212 for treating a range of ailments, making it an area of active scientific inquiry.

How can PubCompare.ai assist researchers in optimizing the use of WIN 55,212 in their studies?

PubCompare.ai's AI-powered protocol comparison tool can help researchers streamline their work with WIN 55,212. The platform allows you to efficiently screen protocol literature, leveraging AI to pinpoint critical insights. By comparing the effectiveness of different protocols related to WIN 55,212, the tool can enable you to identify the most suitable option for your specific research goals, improving reproducibility and accuracy. PubCompare.ai's cutting-edge technology can be a valuable asset in navigating the complexities of working with this intriguing synthetic cannabinoid.

Are there any common challenges or considerations when using WIN 55,212 in research?

One common challenge when using WIN 55,212 is ensuring proper handling and safety protocols, as it is a potent synthetic cannabinoid. Researchers must be mindful of dosing, administration routes, and potential off-target effects. Additionally, the availability and quality of WIN 55,212 sourced from different suppliers can vary, so it's important to carefully verifty the purity and potenty of the compound used in experiments. By levergiing PubCompare.ai's protocol comparison capabilities, researchers can idnetify the most reliable and well-established methods for working with WIN 55,212, mitigating these potential issues.

Are there any different variations or formulations of WIN 55,212 that researchers should be aware of?

Yes, there are a few different variations and formulations of WIN 55,212 that researchers should be familiar with. The most common form is the racemic mixture, which contains both the active (R)- and inactive (S)-enantiomers. Some studies have also explored the use of the pure (R)-enantiomer, which is thought to be the primary mediator of WIN 55,212's pharmacological effects. Additionally, researchers have investigated different delivery methods, such as topical formulations and nanoparticle-based systems, to enhance the compound's bioavailability and therapeutic potential. Staying up-to-date on the latest developments in WIN 55,212 variations can help researchers select the most appropriate form for their specific research needs.

More about "WIN 55,212"

WIN 55,212 is a synthetic cannabinoid receptor agonist with a range of therapeutic applications.
It acts primarily on the CB1 and CB2 receptors, modulating endocannabinoid signaling pathways and demonstrating potent analgesic, anti-inflammatory, and neuroprotective effects in preclinical models.
Closely related compounds include WIN 55,212-2, AM251, and CP55,940, which share similar pharmacological profiles and have also been studied for their potential therapeutic benefits.
WIN 55,212 has shown promise in the treatment of pain, neurological disorders, and other conditions, making it an area of ongoing research and development.
Researchers often utilize DMSO and Tween 80 as solvents and vehicles for administering WIN 55,212 and related compounds in experimental settings.
The mesylate salt form of WIN 55,212-2 has also been investigated, potentially offering improved solubility and bioavailability.
As scientists and clinicians continue to explore the therapeutic potential of WIN 55,212 and its analogues, the field of endocannabinoid research remains an active and promising area of study.