Product Name Reticuline
CAS No.: 485-19-8
Catalog No.: CFN98767
Molecular Formula: C19H23NO4
Molecular Weight: 329.4 g/mol
Purity: >=98%
Type of Compound: Alkaloids
Physical Desc.: Oil
Targets: Calcium Channel
Source: The roots of Thalictrum foliolosum
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Reticuline is a key compound in the biosynthetic pathway for isoquinoline alkaloids in plants, which include morphine, codeine and berberine. Reticuline possesses potent central nervous system depressant action, it (50-100 mg/kg i.p.) can produce alteration of behaviour pattern, prolongation of pentobarbital-induced sleep, reduction in motor coordination and D-amphetamine-induced hypermotility and suppression of the conditioned avoidance response. (S)-Reticuline can elicit vasorelaxation probably due to the blockade of the L-type voltage-dependent Ca(2+) current in rat aorta, the effect may contribute to the potential cardioprotective efficacy of (S)-reticuline.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

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The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Transgenic Res. 2007 Jun;16(3):363-75.
    Knockdown of berberine bridge enzyme by RNAi accumulates (S)-reticuline and activates a silent pathway in cultured California poppy cells.[Pubmed: 17103244 ]
    Reticuline is a key compound in the biosynthetic pathway for isoquinoline alkaloids in plants, which include morphine, codeine and berberine.
    We established cultured California poppy (Eschscholzia californica) cells, in which berberine bridge enzyme (BBE) was knocked down by RNA interference, to accumulate the important key intermediate Reticuline. Both BBE mRNA accumulation and enzyme activity were effectively suppressed in transgenic cells. In these transgenic cells, end-products of isoquinoline alkaloid biosynthesis, such as sanguinarine, were considerably reduced and Reticuline was accumulated at a maximum level of 310 mug/g-fresh weight. In addition, 1 g-fresh weight of these cells secreted significant amounts of Reticuline into the medium, with a maximum level of 6 mg/20 mL culture medium. These cells also produced a methylated derivative of Reticuline, laudanine, which could scarcely be detected in control cells.
    We discuss the potential application of RNAi technology in metabolic modification and the flexibility of plant secondary metabolism.
    Med Sci Monit. 2005 May;11(5):MS1-5.
    In vivo and in vitro L-DOPA and reticuline exposure increases ganglionic morphine levels.[Pubmed: 15874894]
    Given the presence of morphine, its metabolites and precursors, i.e., Reticuline, in mammalian and invertebrate tissues, it has become imperative to determine if exposing tissues to putative opiate alkaloid and dopamine precursors would result in increasing endogenous morphine levels.
    Endogenous morphine levels were determined by high performance liquid chromatography coupled to electrochemical detection and radioimmunoassay, following incubation of Mytilus edulis pedal ganglia with Reticuline or L-DOPA. Injection of L-DOPA or Reticuline into healthy animals was via the foot. Ganglia incubated in vitro with Reticuline or L-DOPA for 1 hour exhibited a concentration and time dependent statistically significant increase in their endogenous morphine levels (5.0 +/- 0.47, 3.6 +/- 0.45 ng/ganglion, respectively). Injection of intact, healthy animals with Reticuline or L-DOPA also results in significantly higher endogenous ganglionic morphine levels.
    Taken together, we show that L-DOPA is being converted to morphine, demonstrating that pedal ganglia can synthesize morphine from these putative precursors in vitro and in vivo. This is the first demonstration of morphine being synthesized in a normal, healthy free living animal.
    J Ethnopharmacol. 1998 Aug;62(1):57-61.
    Central depressant effects of reticuline extracted from Ocotea duckei in rats and mice.[Pubmed: 9720612]

    Neuropharmacological studies were carried out with Reticuline, a benzylisoquinoline alkaloid, isolated from Ocotea duckei Vattimo. It was found that Reticuline (50-100 mg/kg i.p.) produced alteration of behaviour pattern, prolongation of pentobarbital-induced sleep, reduction in motor coordination and D-amphetamine-induced hypermotility and suppression of the conditioned avoidance response.
    These observations suggest that Reticuline possesses potent central nervous system depressant action.
    Planta Med . 2018 Jan;84(1):20-25.
    Anti-Inflammatory Effects of Boldine and Reticuline Isolated from Litsea cubeba through JAK2/STAT3 and NF-κB Signaling Pathways[Pubmed: 28651290]
    Abstract The anti-inflammatory effects of boldine and Reticuline isolated from Litsea cubeba were evaluated by using xylene-induced ear edema and carrageenan-induced paw edema in mice and rats. Our results demonstrated that intragastric administration with boldine and Reticuline significantly mitigated ear weight in mice and decreased paw volume in rats. A combination administration of boldine (0.5 mg/kg) + Reticuline (0.25 mg/kg) resulted in a potentiated inhibition in these two models. In parallel, boldine or Reticuline reduce the infiltration of neutrophil leukocytes in rat paw tissue, respectively, and the combination of the two groups performed a better anti-inflammatory activity as shown in histopathologies. Boldine, Reticuline, and their combination notably inhibited mRNA expressions of TNF-α, and IL-6 and reduced the phosphorylation levels of Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3). Beyond that, their combination also can reduce the phosphorylation levels of p65 and IκBα in the pathological tissues of animals, as observed by real-time PCR and western blot analyses, respectively. These findings indicate for the first time that boldine and Reticuline have not only anti-inflammatory activity but also potential synergistic effects in vivo. The underlying mechanism may relate to the inhibition on the expression of pro-inflammatory cytokines, such as TNF-α and IL-6, which may be a consequence of JAK2/STAT3 and NF-κB pathway involvements. This study provides useful data for further exploration and application of boldine and Reticuline as potential anti-inflammatory medicines.
    Naunyn Schmiedebergs Arch Pharmacol. 2009 Feb;379(2):115-25.
    (S)-reticuline induces vasorelaxation through the blockade of L-type Ca(2+) channels.[Pubmed: 18825370]
    In Brazil, various species of the genus Ocotea are used in folk medicine for treating several diseases. The chemical characterization of this plant showed the presence of alkaloids belonging to the benzyltetrahydroisoquinoline family, the major component of which is (S)-Reticuline.
    The present study investigated whether (S)-Reticuline exerts an inhibitory effect on smooth muscle L-type Ca(2+) channels. Tension measurements and patch clamp techniques were utilized to study the effects of (S)-Reticuline. Whole-cell Ca(2+) currents were measured using the A7r5 smooth muscle cell line. (S)-Reticuline antagonized CaCl(2)- and KCl-induced contractions and elicited vasorelaxation. It also reduced the voltage-activated peak amplitude of I (Ca,L) in a concentration-dependent manner. (S)-Reticuline did not change the characteristics of current density vs. voltage relationship. (S)-Reticuline shifted leftwards the steady-state inactivation curve of I (Ca,L). The application of dibutyryl cyclic adenosine monophosphate to the cell decreased the amplitude of Ca(2+) currents. In cells pretreated with forskolin, an adenylate cyclase activator, the addition of (S)-Reticuline caused further inhibition of the Ca(2+) currents suggesting an additive effect.
    The results obtained show that (S)-Reticuline elicits vasorelaxation probably due to the blockade of the L-type voltage-dependent Ca(2+) current in rat aorta. The reported effect may contribute to the potential cardioprotective efficacy of (S)-Reticuline.
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