Fig. 1 · Structure

Documents & Downloads

Methocarbamol

Nav1.4 Channel Blocker

Methocarbamol is a central muscle relaxant that functions as a Nav1.4 channel blocker. It reversibly modulates the voltage dependence of Nav1.4 channel inactivation, providing insights into neuromuscular transmission. This compound is valuable for research into muscle spasms and pain syndromes, making it a pertinent tool for studies focused on neuromuscular disorders and related therapeutic interventions.

In Stock

Free Aliquoting for Your Order

Tell us your preferred amount per vial. We’ll confirm the options.

In Vitro Studies

In SH-SY5Y cells incubated in complete medium, 30 μM Methocarbamol produced a time-dependent increase in cathepsin D levels in the cell medium. The drug-induced increase was abrogated by VAMP7 or ARL8B inhibition. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Methocarbamol increases extracellular cathepsin D in cultured cells

Cell-based study · SH-SY5Y cells [1]

SH-SY5Y cells incubated in complete medium with 30 μM Methocarbamol showed a time-dependent increase in cathepsin D levels in the cell medium. The drug-induced increase was abrogated by VAMP7 or ARL8B inhibition.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Levels of cathepsin D released into the cell mediumReported result SH-SY5Y cells incubated in complete medium with 30 μM methocarbamol showed a time-dependent increase in cathepsin D levels in the cell medium; the drug-induced increase in extracellular cathepsin D was abrogated by VAMP7 or ARL8B inhibition.[1]

Literature-Reported Treatment Conditions

Treatment concentration
30 μM
Exposure duration
over 12 h
Method
incubated in complete medium
Vehicle
0.1% DMSO
Methods and source locations

Compound reported in the paper: Methocarbamol

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Results > CA inhibition induces tau secretion by lysosomal exocytosis (S74, S85); Methods > Cell-based experiments > ELISA analysis of cathepsin D in cell medium (S284, S285, S287); Fig. 4 legend (S512)

Levels of cathepsin D released into the cell medium: Levels of cathepsin D released into the cell medium; comparator: control samples treated with DMSO at 4 h — Results > CA inhibition induces tau secretion by lysosomal exocytosis (S74, S85); Methods > Cell-based experiments > ELISA analysis of cathepsin D in cell medium (S284)

In Vivo Studies

In rho:eGFP–tau-WT heterozygous fish, Methocarbamol at 10 μM added to each well increased the zpr-3:zpr-1 ratio by 457.9% compared with water control. The design also included phenylthiourea (PTU), with the compound effect isolated by comparison with water control. [1]

Methocarbamol increases the zpr-3:zpr-1 ratio in fish

Animal study · rho:eGFP–tau-WT heterozygous fish [1]

In rho:eGFP–tau-WT heterozygous fish, Methocarbamol at 10 μM added to each well increased the zpr-3:zpr-1 ratio by 457.9% compared with water control. The design also included phenylthiourea (PTU), with the compound effect isolated by comparison with water control.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
zpr-3:zpr-1 ratiozpr-3:zpr-1 ratio 10 μM: increase in the zpr-3:zpr-1 ratio of 457.9%[1]

Conditions shared by the study groups

Route
added to each well
Vehicle
water
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Methocarbamol 10 μMwater controlincrease in the zpr-3:zpr-1 ratio of 457.9%[1]
Methocarbamol 10 μM
Model: rho:eGFP–tau-WT heterozygous fish
Reported limits: Not stated in the sentences used: schedule.
Methods and source locations

Compound reported in the paper: Methocarbamol

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Results > Identification of methocarbamol from the compound screen (S15); Methods > Zebrafish experiments > Experimental crosses (S140); Methods > Zebrafish experiments > Primary screen > Treatments with compound library (S156); Extended Data Fig. 2 legend (S401, S402)

zpr-3:zpr-1 ratio: zpr-3:zpr-1 ratio; comparator: water control — Results > Identification of methocarbamol from the compound screen (S15); Methods > Zebrafish experiments > Primary screen > Treatments with compound library (S156); Extended Data Fig. 2 legend (S401)

Methocarbamol 10 μM · Results > Identification of methocarbamol from the compound screen (S15); Methods > Zebrafish experiments > Primary screen > Treatments with compound library (S156); Extended Data Fig. 2 legend (S401)

Specifications

Manufacturer Adooq Bioscience
Actions Blocker
CAS Number 532-03-6
Applications Nav1.4 Channel Blocker
Formula C11H15NO5
Molecular Weight 241.24
SMILES
OC(COC1=CC=CC=C1OC)COC(N)=O

Storage & Solubility

In Vitro Solubility

Reported Solubility

No reported solubility data are available for this product.

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Lopez A, Siddiqi FH, Villeneuve J, et al. Carbonic anhydrase inhibition ameliorates tau toxicity via enhanced tau secretion. Nat Chem Biol (2025). PMID: 39482469 DOI: 10.1038/s41589-024-01762-7 Source material

Added to your cart

View Cart Checkout
Loading...