alpha-Yohimbine

alpha-Yohimbine
Product Name alpha-Yohimbine
CAS No.: 131-03-3
Catalog No.: CFN99400
Molecular Formula: C21H26N2O3
Molecular Weight: 354.5 g/mol
Purity: >=98%
Type of Compound: Alkaloids
Physical Desc.: Powder
Targets: 5-HT Receptor
Source: The barks of Pausinystalia yohimbe
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price:
Alpha-Yohimbine is a 5-HT1A receptor agonist, it is strong selective 2-adrenoceptor antagonist. Alpha-Yohimbine possess aphrodisiac effect.
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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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  • alpha-Yohimbine

    Catalog No: CFN99400
    CAS No: 131-03-3
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    Arch Int Pharmacodyn Ther. 1986 Feb;279(2):212-22.
    A comparison of the binding characteristics of the alpha 2-adrenoceptor antagonists 3H-yohimbine and 3H-rauwolscine in bovine teat muscles.[Pubmed: 2870688]

    METHODS AND RESULTS:
    3H-Yohimbine and alpha-Yohimbine, both potent and selective alpha 2-adrenergic antagonists, were used to identify alpha 2-adrenoceptors in smooth muscles of the cistern wall of teats of lactating cows. Binding of these radioligands was rapid and readily reversed by 10 microM phentolamine. Saturation experiments in the presence of 3H-yohimbine showed an equilibrium KD value of 6.23 +/- 0.74 nM and a maximum number of sites of 81 +/- 7 fmol/mg of membrane protein. In the presence of alpha-Yohimbine , however, a higher density of alpha 2-receptors (164 +/- 12 fmol/mg protein) with a KD of 6.16 +/- 0.64 nM was found. No cooperative interactions among both binding sites were observed. Both 3H-yohimbine and alpha-Yohimbine binding sites showed alpha 2-adrenergic specificity.
    CONCLUSIONS:
    On the basis of its higher affinity to the alpha 2-adrenoceptor sites, better ratio of specific to non-specific binding and for other reasons, alpha-Yohimbine appears to be the ligand of choice.
    Eur J Pharmacol. 1991 May 25;207(1):1-8.
    [3H]rauwolscine behaves as an agonist for the 5-HT1A receptors in human frontal cortex membranes.[Pubmed: 1680719]
    The alpha 2 adrenergic antagonist alpha-Yohimbine binds with comparable nanomolar affinity to alpha 2 adrenoceptors and the nonadrenergic 5-HT1A receptors sites in human frontal cortex membranes.
    METHODS AND RESULTS:
    Addition of 0.5 mM GTP into the incubation medium produces a significant decrease in the amount of alpha-Yohimbine binding sites (Bmax = 230 +/- 16 and 115 +/- 11 fmol/mg protein in the absence and presence of GTP, respectively). The affinity for alpha-Yohimbine remains unchanged (i.e. KD = 40 +/- 0.9 nM and 4.1 +/- 1 nM). This effect of GTP can be attributed to decreased binding of the radioligand to the 5-HT1A receptors. GTP decreases binding of alpha-Yohimbine to nearly the same level as the one corresponding to the alpha 2 adrenoceptors in membranes from both the human frontal cortex and hippocampus. The venom of the marine cone snail, Conus tessulatus, preferentially inhibits alpha-Yohimbine binding to 5-HT1A receptors as compared with the alpha 2 adrenoceptors. Following complete masking of the 5-HT1A receptors by this venom. GTP no longer affects the saturation binding characteristics of alpha-Yohimbine for the remaining alpha 2 adrenoceptors. Nucleotides decrease the binding of alpha-Yohimbine to the 5-HT1A receptors with an order of potencies (i.e. GTP gamma S greater than GPP(NH)P much greater than GDP greater than GTP much greater than ATP) that is typical for nucleotide-mediated receptor-G protein dissociation.
    CONCLUSIONS:
    This suggests that alpha-Yohimbine is a 5-HT1A receptor agonist and this conclusion is compatible with earlier functional studies, indicating that rauwolscine (as well as yohimbine) has agonistic properties at the level of 5-HT autoreceptors.
    Naunyn Schmiedebergs Arch Pharmacol. 1998 Jan;357(1):17-24.
    [3H]Rauwolscine: an antagonist radioligand for the cloned human 5-hydroxytryptamine2b (5-HT2B) receptor.[Pubmed: 9459568]
    In previous reports, [3H]5-HT has been used to characterize the pharmacology of the rat and human 5-HT2B receptors. 5-HT, the native agonist for the 5-HT2B receptor, has a limitation in its usefulness as a radioligand since it is difficult to study the agonist low-affinity state of a G protein-coupled receptor using an agonist radioligand.
    METHODS AND RESULTS:
    When using [3H]5-HT as a radioligand, rauwolscine was determined to have relatively high affinity for the human receptor (Ki human = 14.3+/-1.2 nM, compared to Ki rat = 35.8+/-3.8 nM). Since no known high affinity antagonist was available as a radioligand, these studies were performed to characterize alpha-Yohimbine as a radioligand for the cloned human 5-HT2B receptor expressed in AV12 cells. When alpha-Yohimbine was initially tested for its usefulness as a radioligand, complex competition curves were obtained. After testing several alpha2-adrenergic ligands, it was determined that there was a component of alpha-Yohimbine binding in the AV12 cell that was due to the presence of an endogenous alpha2-adrenergic receptor. The alpha2-adrenergic ligand efaroxan was found to block alpha-Yohimbine binding to the alpha2-adrenergic receptor without significantly affecting binding to the 5-HT2B receptor and was therefore included in all subsequent studies. In saturation studies at 37 degrees C, alpha-Yohimbine labeled a single population of binding sites, Kd = 3.75+/-0.23 nM. In simultaneous experiments using identical tissue samples, alpha-Yohimbine labeled 783+/-10 fmol of 5-HT2B receptors/mg of protein, as compared to 733+/-14 fmol of 5-HT2B receptors/mg of protein for [3H]5-HT binding. At 0 degrees C, where the conditions for [3H]5-HT binding should label mostly the agonist high affinity state of the human 5-HT2B receptor, alpha-Yohimbine (Bmax = 951+/-136 fmol/mg), again labeled significantly more receptors than [3H]5-HT (Bmax = 615+/-34 fmol/mg). The affinity of alpha-Yohimbine for the human 5-HT2B receptor at 0 degrees C did not change, Kd = 4.93+/-1.27 nM, while that for [3H]5-HT increased greatly (Kd at 37 degrees C = 7.76+/-1.06 nM; Kd at 0 degrees C = 0.0735+/-0.0081 nM). When using [3H]rauwolscine as the radioligand, competition curves for antagonist structures modeled to a single binding site, while agonist competition typically resulted in curves that best fit a two site binding model. In addition, many of the compounds with antagonist structures displayed higher affinity for the 5-HT2B receptor when alpha-Yohimbine was the radioligand. Typically, approximately 85% of alpha-Yohimbine binding was specific binding.
    CONCLUSIONS:
    These studies display the usefulness of alpha-Yohimbine as an antagonist radioligand for the cloned human 5-HT2B receptor. This should provide a good tool for the study of both the agonist high- and low-affinity states of the human cloned 5-HT2B receptor.
    Eur J Pharmacol. 1981 Dec 17;76(4):461-4.
    [3H]rauwolscine (alpha-yohimbine): a specific antagonist radioligand for brain alpha 2-adrenergic receptors.[Pubmed: 6276200 ]
    alpha-Yohimbine , a specific and potent alpha 2-antagonist radioligand, was used to characterize alpha 2-receptor binding in bovine cerebral cortex.
    METHODS AND RESULTS:
    alpha-Yohimbine binding was reversible, stereospecific, and saturable. Association, dissociation, and saturation studies revealed one site interactions (k -1/k+1 = 1.2 nM, KD = 2.5 nM, Bmax = 160 fmol/mg protein) and competition studies indicated that alpha-Yohimbine labeled the alpha 2-receptor. Agonists inhibited alpha-Yohimbine binding in a shallow, GTP-sensitive manner.
    CONCLUSIONS:
    These results suggest that alpha-Yohimbine specifically labels both the high and low affinity states of the alpha 2-receptor in brain membranes.
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