Catalog No.S4023 Synonyms: Novocaine HCl
Molecular Weight(MW): 272.77
Procaine is an inhibitor of sodium channel, NMDA receptor and nAChR with IC50 of 60 μM, 0.296 mM and 45.5 μM, which is also an inhibitor of 5-HT3 with KD of 1.7 μM.
1 Customer Review
Procaine pretreatment inhibits JAK2 and STAT3 expression. (A) Relative Jak2 mRNA level detected by qRT-PCR. (B) Relative Stat3 mRNA level detected by qRT-PCR. (C) JAK2 and STAT3 protein expression detected by western blot. (D) Relative protein levels of JAK2 and STAT3 based on Western blot results. sham, rats undergone sham surgery. CCI, rats undergone sciatic nerve chronic compression injury (CCI) as the neuropathic pain (NPP) model. CCI+procaine, NPP model rats pretreated with procaine. The detection is performed on the 20th day post surgery (n=3). GAPDH is used as an internal reference. *p<0.05, **p<0.01. JAK2, Janus kinase 2. STAT3, signal transducer and activator of transcription 3.
Biomol Ther (Seoul), 2016, 24(5): 489-494.. Procaine HCl purchased from Selleck.
Purity & Quality Control
Choose Selective Sodium Channel Inhibitors
Click to view more
2. For more details, such as half maximal inhibitory concentrations (IC50s) and working concentrations of each inhibitor, please click on the link of the inhibitor of interest.
3. "+" indicates inhibitory effect. Increased inhibition is marked by a higher "+" designation.
4. Orange "√" refers to compounds which do inhibitory effects on the related isoform, but without specific value.
|Description||Procaine is an inhibitor of sodium channel, NMDA receptor and nAChR with IC50 of 60 μM, 0.296 mM and 45.5 μM, which is also an inhibitor of 5-HT3 with KD of 1.7 μM.|
Procaine acts mainly by inhibiting sodium influx through voltage gated sodium channels in the neuronal cell membrane of peripheral nerves. When the influx of sodium is interrupted, an action potential cannot arise and signal conduction is thus inhibited. The receptor site is thought to be located at the cytoplasmic (inner) portion of the sodium channel.  Procaine has also been shown to bind or antagonize the function of N-methyl-D-aspartate (NMDA) receptors  as well as nicotinic acetylcholine receptors  and the serotonin receptor-ion channel complex.  Procaine is an inhibitor of the mechanisms of Ca-induced Ca release and caffeine-induced Ca release in various types of muscle preparations. 0.5 mM Procaine blocks individual sarcoplasmic reticulum Ca2+ release channels in planarlipid bilayers. Procaine does not reduce the single channel conductance nor appreciably shorts the mean open times of the channel, rather, it increases the longest closed time.  Procaine is a DNA-demethylating agent with growth-inhibitory effects in human cancer cells. 0.5 mM Procaine produces a 40% reduction in 5-methylcytosine DNA in MCF-7 breast cancer cell line. Procaine can also bind to CpG-enriched DNA, and demethylates densely hypermethylated CpG islands, leading to restoring gene expression of epigenetically silenced genes. Procaine treatment (0.5 mM) induces an increase in the mitotic index of cells in M phase. Procaine treatment (1 mM) reduces cell proliferation by ~40%.  Procaine influences red cell shape and deformability. 45 mM Procaine almost completely prevents the discocyte-echinocyte transformation associated with ATP depletion. Similar concentrations of Procaine normalize the viscosity and filterability, but have no effect on cell volume, osmotic fragility, or monovalent cation composition of cells undergoing ATP depletion. 
|In vivo||Procaine is an excitant of limbic system cells. 15 mg/kg Procaine increases cellular activity in amygdala ventral hippocampus, nucleus accumbens, temporal neocortex and ventromedial hypothalamus of awaken cat. Procaine facilitates transmission of evoked excitatory activity from the amygdala to the ventromedial hypothalamus.  Procaine influences frequency and amplitude of reticularly elicited hippocampal rhythmical slow activity. Procaine (0.5 μL, 20% wt/vol) injected at points in the ascending system anterior to the supramamillary nucleus, in the region of the medial forebrain bundle or in the medial septum, reduces the amplitude of reticularly elicited rhythmical slow activity (RSA) but has no effect on its frequency. Procaine injected at points in the ascending system from just anterior to the reticular formation stimulation site, up to, and including the supramamillary nucleus, reduces both the frequency and amplitude of reticularly elicited RSA.  Procaine (80mg/kg) increases the duration and propagation of epileptiform afterdischarges (ADs) produced by electrical stimulation of the amygdala in rats. Porcaine also increases the rate of seizure development (kindling) produced by repeated stimulation of the amygdala. Procaine would itself act as convulsants in well kindled subjects. Procaine produces a weak but significant increase in the amplitude of the transcallosal evoked potential.  Procaine influences generation of auditory brain stem responses (ABRs). Procaine (30 μL of 1% solution) injection into the trapezoid body of guinea pig affects many of the components of the scalp-derived ABR: N2 is delayed making P2 broader in duration, P3 and N3 are lost, P4 is shortened in latency, broadened in duration but unaffected in amplitude, and N4 is considerably attenuated. Only P1 and N1 are unaffected by the procaine injection.  Procaine increases the therapeutic index of cisplatin by improving antitumor activity of cisplatin and reducing its nephrotoxicity. Simultaneous administration of cisplatin and Procaine (40 mg/kg) to BDF1 mice produces 50% lethal dose (LD50) and 90% lethal dose (LD90) values approximately two times higher than those observed with cisplatin alone. Simultaneous administration produces a higher cure rates compared with cisplatin alone (50% vs 9%). The increased blood urea nitrogen (BUN) levels observed 4-7 days following a single administration of cisplatin, as well as the tubular degenerative changes detected by light microscopy, are not observed when the same doses of cisplatin are given simultaneously with Procaine. |
-  Br?u ME, et al. Anesth Analg, 1998, 87(4), 885-889.
-  Hahnenkamp K, et al. Br J Anaesth, 2006, 96(1), 77-87.
-  Wang H, et al. Eur J Pharmacol, 2010, 630(1-3), 29-33.
-  Fan P, et al. Neuropharmacology, 1994, 33(12), 1573-1579.
-  Zahradn韐ov?A, et al. Biophys J, 1993, 64(4), 991-1
-  Villar-Garea A, et al. Cancer Res, 2003, 63(16), 4984-4989.
-  Palek J, et al. Blood, 1977, 50(1), 155-164.
-  Adamec RE, et al. Prog Neuropsychopharmacol Biol Psychiatry, 1987, 11(4), 345-364.
-  Kirk IJ, et al. Hippocampus, 1993, 3(4), 517-525.
-  Racine R, et al. Electroencephalogr Clin Neurophysiol, 1975, 38(4), 355-365.
-  Wada SI, et al. Electroencephalogr Clin Neurophysiol, 1983, 56(4), 326-339
-  Esposito M, et al. J Natl Cancer Inst, 1990, 82(8), 677-684.
|In vitro||DMSO||55 mg/mL (201.63 mM)|
|Water||55 mg/mL (201.63 mM)|
* 1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:
Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)
*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).
Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )
* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).
Molecular Weight Calculator
Enter the chemical formula of a compound to calculate its molar mass and elemental composition:
Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2
Instructions to calculate molar mass (molecular weight) of a chemical compound:
To calculate molar mass of a chemical compound, please enter its chemical formula and click 'Calculate'.
Definitions of molecular mass, molecular weight, molar mass and molar weight:
Molecular mass (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.
Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT02726620||Recruiting||Hypotension||Vanderbilt University Medical Center|UMC Utrecht||January 2017||--|
|NCT02919072||Not yet recruiting||Unplanned Caesarean Section||Sintetica SA|Cross Research S.A.|Aml Research||October 2016||Phase 3|
|NCT02862912||Not yet recruiting||Adverse Reaction to Spinal Anesthetic|Maternal Care for Cervical Incompetence||Columbia University||August 2016||Phase 4|
|NCT02735317||Not yet recruiting||Nasopharyngeal Neoplasms|Stomatitis||Yun-fei Xia|Sun Yat-sen University||April 2016||Phase 2|
|NCT03038958||Completed||Knee Arthroscopy|Spinal Anesthesia||Centre Hospitalier Universitaire Saint Pierre|Hôpital de Braine-lAlleud||April 2016||Phase 4|
|NCT02528123||Recruiting||Myopia|Refractive Errors||London Vision Clinic||April 2016||--|
Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.
Tel: +1-832-582-8158 Ext:3
If you have any other enquiries, please leave a message.