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    Procaine HCl (Novocaine)
    Procaine HCl (Novocaine)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1666
    CAS #: 51-05-8Purity ≥98%

    Description: Procaine HCl (also known as Novocaine; Gerovital H3; Aminocaine), the HCl salt of Procaine, is a local anesthetic that acts as an inhibitor of sodium channel, NMDA receptor and nAChR with IC50 of 60 μM, 0.296 mM and 45.5 μM. Procaine 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. 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.

    References: Anesth Analg. 1998 Oct;87(4):885-9; Br J Anaesth. 2006 Jan;96(1):77-87.

    Related CAS #: 51-06-9 (free base)   51-05-8 (HCl) 

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    Molecular Weight (MW)272.77 
    CAS No.51-05-8 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 55 mg/mL (201.6 mM) 
    Water: 55 mg/mL (201.6 mM) 
    Ethanol: <1 mg/mL
    Solubility (In vivo)

    Chemical Name: 2-(diethylamino)ethyl 4-aminobenzoate;hydrochloride


    InChi Code: InChI=1S/C13H20N2O2.ClH/c1-3-15(4-2)9-10-17-13(16)11-5-7-12(14)8-6-11;/h5-8H,3-4,9-10,14H2,1-2H3;1H

    SMILES Code: CCN(CC)CCOC(=O)C1=CC=C(C=C1)N.Cl           

    SynonymsNovocaine HCl; Procaine Hydrochloride; Procaine HCl; Novocaine hydrochloride; Gerovital H3; Aminocaine

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    In Vitro

    In vitro activity: 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 VivoProcaine 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. 
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    Anesth Analg. 1998 Oct;87(4):885-9; Br J Anaesth. 2006 Jan;96(1):77-87; Prog Neuropsychopharmacol Biol Psychiatry. 1987;11(4):345-64; Hippocampus. 1993 Oct;3(4):517-25; Electroencephalogr Clin Neurophysiol. 1975 Apr;38(4):355-65. 

    These protocols are for reference only. InvivoChem does not independently validate these methods.


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