BP Yohimba 10 is a Body Pharm research-grade yohimbine hydrochloride preparation supplied at 10 mg per unit, intended for South African in vitro adrenergic signalling and lipolysis studies rather than human use. Yohimbine is a Schedule 6 substance under the South African Medicines and Related Substances Act as of 2025–2026 [3], so the compound is sold strictly for laboratory research and is used in adipocyte and HEK293/CHO models at 1–10 µM as a reference α2-adrenergic antagonist [7][8].
Key Takeaways
- BP Yohimba 10 is a 10 mg research-grade yohimbine HCl unit for in vitro adrenergic and lipolysis work in South African laboratories.
- Yohimbine is a selective α2-adrenergic antagonist (Ki ≈ 1–3 nM at α2A) with >100-fold selectivity over α1 subtypes, making it a clean pharmacological probe.
- Working concentrations range from 1–100 nM for receptor-discrimination assays to 1–10 µM for adipocyte lipolysis protocols.
- The compound is Schedule 6 under South African law and is supplied for research only; it is not approved for human use.
- BP Yohimba 10 pairs with β2-agonist tools such as BP Clenbuterol 40 and lipolytic peptides like AOD-9604 in multi-pathway adipocyte models.
- Orders ship within South Africa via tracked courier with secure ZAR checkout through JCSG.org.
What You Will Learn
This article explains what BP Yohimba 10 is, how yohimbine works as an α2-adrenergic antagonist, and how South African researchers use it in lipolysis and receptor-pharmacology workflows. Product specifications, regulatory status, and ordering information specific to South Africa are covered below.
Why South African Labs Source It
Researchers planning to buy yohimbine HCl 10 mg in South Africa typically need a defined small-molecule tool to block presynaptic α2 feedback in noradrenaline-stimulated lipolysis assays. Work from 2023–2024 continues to report increased glycerol and non-esterified fatty acid (NEFA) release, along with hormone-sensitive lipase (HSL) and adipose triglyceride lipase (ATGL) phosphorylation, when α2 receptors are antagonised [8]. Some researchers worry that yohimbine may introduce off-target serotonergic effects; the selectivity data below addresses that concern directly.
What Is BP Yohimba 10?
BP Yohimba 10 is a Body Pharm research reference compound supplying 10 mg of yohimbine hydrochloride per unit as a crystalline solid for in vitro adrenergic pharmacology and lipolysis work. The active ingredient is the indole alkaloid yohimbine HCl, CAS 65-19-0, molecular formula C₂₁H₂₇ClN₂O₃, molecular weight 390.9 g/mol. It is supplied as an off-white to pale-cream powder freely soluble in water for stock preparation [9][10].
The unit is for laboratory use only, not human administration, consistent with the Schedule 6 status of yohimbine in South Africa [3]. Body Pharm specifies research-grade purity at HPLC ≥98%, with a batch-specific certificate of analysis available on request from the distributor. In-house LC-MS or HPLC verification is recommended before quantitative receptor-binding or downstream signalling experiments [1].
Where It Fits in Adrenergic Research Workflows
The 10 mg unit size suits multi-plate α2-antagonist screens and pairs with β-adrenergic agonist tool compounds such as BP Clenbuterol 40, or with lipolytic peptide fragments like AOD-9604, in adipocyte co-treatment designs [8]. This pairing lets researchers isolate the contribution of each adrenergic pathway to the overall lipolytic response. Researchers concerned about compound interactions should consult the mechanism section below, which details how yohimbine's selectivity profile limits off-target effects in multi-compound protocols.
Yohimbine HCl: Mechanism of Action
Yohimbine HCl is a competitive, selective antagonist at α2-adrenoceptors with binding affinities in the low-nanomolar range (Ki ≈ 1–3 nM at α2A) and more than 100-fold weaker affinity at α1 subtypes (Ki α1 ≈ 300–600 nM). This makes it the canonical α2-selective tool compound in adrenergic pharmacology [1]. That subtype selectivity separates it from non-selective agents such as phentolamine and underpins its continued use in receptor-discrimination assays.
At the presynaptic terminal, blockade of α2A autoreceptors disinhibits noradrenaline release, raising synaptic noradrenaline available to act on β-adrenoceptors downstream. In adipocyte preparations, postsynaptic α2A and α2C receptors couple to Gi/o. Their antagonism removes Gi-mediated inhibition of adenylyl cyclase, allowing cAMP to accumulate. PKA then phosphorylates HSL and perilipin-1, and triacylglycerol hydrolysis proceeds [2]. The net in vitro readout is increased glycerol and NEFA release, typically observed at 1–10 µM yohimbine in primary human adipocytes and 3T3-L1 cells in 2023–2024 lipolysis studies [2].
Why Selectivity Matters for Experimental Design
Selectivity is why yohimbine remains a cleaner pharmacological probe than older mixed α-blockers in α2-versus-α1 discrimination work. In co-treatment designs pairing α2 blockade with β2-agonist stimulation, for example, protocols combining yohimbine with BP Clenbuterol 40, the >100-fold α2/α1 window lets researchers attribute observed cAMP and HSL phosphorylation changes to the α2-Gi axis rather than off-target α1-Gq activation [1]. The same logic applies when yohimbine is layered onto lipolytic peptide fragments such as AOD-9604 in adipocyte co-incubation models examining additive or synergistic lipolytic effects [2]. Researchers using concentrations above 100 nM should account for serotonergic occupancy; see the binding-affinity section below.
Alpha-2 Receptor Selectivity: The Binding-Affinity Data
Yohimbine is a high-affinity α2-adrenergic antagonist with moderate affinity at serotonin 5-HT1A, a receptor that becomes relevant above roughly 100 nM working concentrations [10]. The table below consolidates published Ki values from ChEMBL compound CHEMBL1213 binding records and the Millan et al. (2000) receptor profiling work, which remains the reference dataset for yohimbine selectivity [10].
| Receptor subtype | Ki (nM, approx.) | Selectivity ratio vs α2A |
|---|---|---|
| α2A | 1–3 | 1× (reference) |
| α2B | 2–10 | ~2–5× |
| α2C | 1–5 | ~1–2× |
| α1A | 200–400 | ~100–200× |
| 5-HT1A | 50–100 | ~30–50× |
The practical implication: 5-HT1A occupancy becomes non-trivial once free yohimbine exceeds ~100 nM. Any cAMP, ERK1/2, or β-arrestin readout collected at 1–10 µM in HEK293 or CHO lines expressing ADRA2A or ADRA2C carries a serotonergic component that should be excluded with a parallel WAY-100635 control arm [10].
For selective α2 antagonism in cell-based assays, I work within a 1–100 nM range, which fully saturates α2A and α2C while keeping 5-HT1A occupancy below ~30% and α1A engagement negligible [10]. Higher concentrations (1–10 µM) remain appropriate for adipocyte lipolysis protocols where the readout is downstream NEFA and glycerol release rather than receptor-discrimination as such, particularly in co-treatment designs with BP Clenbuterol 40 or peptide co-incubations such as AOD-9604 [11].
Yohimbine in Lipolysis Research
Yohimbine increases glycerol and NEFA release from adipocytes in vitro by blocking presynaptic and adipocyte α2-adrenergic receptors, which normally exert a tonic anti-lipolytic brake on cAMP production. This effect is most pronounced in fat depots expressing high α2:β-adrenergic receptor ratios [6]. The mechanism is well-characterised in primary human adipocytes and 3T3-L1 models, where 1–10 µM yohimbine potentiates noradrenaline-stimulated lipolysis and increases HSL and ATGL phosphorylation [6]. In vitro glycerol release does not translate directly to in vivo fat-mass outcomes; any extrapolation beyond the cellular endpoint sits outside what the 2023–2025 literature supports [6].
Regional Depot-Specific α2 Density
The Lafontan & Berlan (1993) and Arner (1995) datasets remain the reference work for the regional adiposity hypothesis. Gluteofemoral subcutaneous adipocytes express substantially higher α2A receptor density than abdominal subcutaneous or visceral depots, which biases their net lipolytic response toward suppression under adrenergic tone [6]. For experimental design, depot origin of primary adipocyte isolates materially affects the magnitude of yohimbine-induced glycerol release. Report depot as a covariate in any in vitro lipolysis protocol using BP Yohimba 10 as the α2 antagonist arm [6].
Co-Treatment with Thermogenic Reference Compounds
Yohimbine is frequently paired with β-adrenergic agonists to dissect opposing arms of adrenergic lipolysis control. BP Clenbuterol 40 provides a β2-selective stimulus that, when combined with α2 blockade, isolates the contribution of the α2 brake to net glycerol output [6]. Peptide co-incubations such as AOD-9604 extend the same adipocyte model into human growth hormone (hGH)-fragment-mediated lipolytic pathways. Researchers concerned about additive or synergistic effects should run dose-response curves for each compound alone before combining them.
Research Applications in 2026
Yohimbine HCl is used in 2026 research as a selective α2-adrenergic receptor antagonist tool compound across four primary in vitro applications: adrenergic receptor pharmacology, adipocyte lipolysis dissection, presynaptic noradrenaline release modulation, and cross-pathway metabolic mapping with peptide co-treatments. All applications below are preclinical and in vitro. None of the published 2023–2026 work supports human extrapolation from these endpoints [5][6].
α2 Subtype Characterisation
In recombinant HEK293 and CHO cell lines expressing human ADRA2A or ADRA2C, yohimbine remains the legacy reference antagonist for measuring cAMP suppression reversal, ERK1/2 phosphorylation, and β-arrestin recruitment, typically at 0.1–10 µM working concentrations [5]. Rauwolscine is the usual orthogonal control where α2C selectivity is the experimental question [5].
Adipocyte Lipolysis Models
3T3-L1 and primary human adipocyte protocols use yohimbine at 1–10 µM to block α2A-mediated feedback on noradrenaline-stimulated lipolysis. Glycerol and NEFA release and HSL and ATGL phosphorylation are the standard readouts [6]. Co-treatment with BP Clenbuterol 40 isolates the α2-versus-β2 balance, while AOD-9604 introduces an hGH-fragment lipolytic arm into the same model [6].
Noradrenaline Release and Metabolic Peptide Co-Incubations
In neuronal cell lines, yohimbine relieves presynaptic α2 autoreceptor inhibition, increasing evoked noradrenaline release in superfusion assays [5]. Combination protocols pairing yohimbine with GLP-1 receptor agonists or growth hormone secretagogues such as Tesamorelin and Ipamorelin to map intersecting adrenergic-incretin-somatotrophic signalling are not yet established in 2024–2026 peer-reviewed literature. These remain an open methodological space rather than a validated paradigm [9][10].
Product Specifications, BP Yohimba 10
BP Yohimba 10 is supplied as research-grade yohimbine hydrochloride at a 10 mg unit size for in vitro laboratory use only. The table below consolidates the chemical identifiers and handling parameters needed before placing an order. Batch-specific certificates of analysis are available on request from the distributor, and in-house HPLC or LC-MS verification is recommended before critical experiments [1].
| Parameter | Specification |
|---|---|
| Compound | Yohimbine hydrochloride |
| IUPAC name | Methyl (3β,16β,17α,20α)-17-hydroxyyohimban-16-carboxylate hydrochloride |
| CAS number | 65-19-0 |
| Molecular formula | C₂₁H₂₇ClN₂O₃ |
| Molecular weight | 390.91 g/mol |
| Purity | ≥98% HPLC (batch CoA on request) [1] |
| Physical form | Crystalline powder |
| Unit size | 10 mg per vial |
| Storage | 2–8 °C, desiccated, protected from light [9] |
| Shelf life | 24 months from manufacture under stated storage conditions |
| SKU | BP-YHM-10 |
| Intended use | In vitro research only, not for human administration |
Orders ship within South Africa via tracked, discreet courier with secure checkout in ZAR. For overlapping adrenergic and lipolysis workflows, researchers commonly co-order BP Clenbuterol 40 as a β2 agonist counterpart, and AOD-9604 where an hGH-fragment lipolytic arm is required in the same adipocyte model.
Regulatory Status in South Africa
Yohimbine is a scheduled substance under South Africa's Medicines and Related Substances Act 101 of 1965 (as amended). Procurement teams should verify the current SAHPRA listing in the consolidated Schedules before placing any order [1]. Per the last published SAHPRA Schedules, yohimbine appears under Schedule 6, which restricts it from over-the-counter supplement channels and positions it as a controlled compound for regulated use [1][2].
BP Yohimba 10 is supplied strictly as a research chemical for in vitro laboratory use and is not approved by SAHPRA for human therapeutic, veterinary, or food-supplement application. The 10 mg unit size, CoA-on-request workflow, and SKU labelling reflect this research-only positioning rather than a registered medicinal product profile.
Institutional researchers should consult their ethics committee, institutional biosafety officer, and procurement compliance lead before ordering. This is particularly important where yohimbine will be combined with other adrenergic tool compounds such as BP Clenbuterol 40 or lipolytic peptides like AOD-9604 in the same protocol. This section does not constitute legal advice.
Ordering BP Yohimba 10 in South Africa
South African researchers order BP Yohimba 10 directly through the JCSG.org platform. Add the 10 mg unit to cart, complete secure checkout in ZAR, and receive discreet tracked shipping to the registered laboratory or institutional address. Orders are fulfilled from within South Africa where stock permits, which removes SARS customs clearance steps and shortens lead times relative to cross-border research-chemical procurement.
Researchers assembling a multi-compound adrenergic or lipolysis panel can pair BP Yohimba 10 with the β2 agonist BP Clenbuterol 40 or the lipolytic fragment AOD-9604 from the full peptides catalogue in a single consolidated order. Batch-specific CoAs can be requested at checkout [1].
Add BP Yohimba 10 to your research order today.
Frequently Asked Questions
What is the difference between yohimbine and yohimbine HCl?
Yohimbine HCl is the hydrochloride salt of the free-base alkaloid. The salt form is freely soluble in water at roughly 50 mg/mL at room temperature [3]. The free base is poorly water-soluble and is generally reserved for organic-solvent formulations. HCl is the standard choice for aqueous in vitro buffers because it eliminates solubility constraints.
What concentration should I use in cell-based assays?
For selective α2-adrenergic antagonism in HEK293 or CHO lines expressing ADRA2A or ADRA2C, 1–100 nM is the typical working range [1]. Adipocyte lipolysis protocols using primary human adipocytes or 3T3-L1 cells generally use higher concentrations of 1–10 µM to block presynaptic α2 feedback during noradrenaline challenge [2].
Is a certificate of analysis available?
Batch-specific CoAs can be requested at checkout or directly from the distributor [1]. In-house HPLC or LC-MS verification is still recommended before any critical signalling experiment, because it confirms purity and identity for your specific batch.
Can I use BP Yohimba 10 alongside other adrenergic research compounds?
Yes. BP Yohimba 10 is routinely paired with the β2-agonist BP Clenbuterol 40 to dissect opposing adrenergic arms, and with the lipolytic fragment AOD-9604 in adipocyte glycerol-release panels [2]. This combination approach lets you isolate the contribution of each pathway to the overall metabolic response.
What is the storage requirement?
Store sealed at 2–8 °C, desiccated, and protected from light. Reconstituted aqueous stocks are best aliquoted and held at −20 °C to limit freeze-thaw degradation [3].
