Fig. 1 · Structure

Cat. No.: A13407
CAS No.: 21898-19-1
Formula: C₁₂H₁₈Cl₂N₂O.HCl
Mol. Weight: 313.65

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Clenbuterol hydrochloride

Name: Clenbuterol hydrochloride
Brand: Adooq Bioscience
SKU: A13407
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Cat. No. A13407 CAS 21898-19-1

Clenbuterol Hydrochloride is a sympathomimetic β2-adrenoceptor agonist that has been used as a bronchodilator in the treatment of pulmonary diseases such as asthma. At higher doses, clenbuterol acts as an anabolic steroid, favoring skeletal muscle protein synthesis at the expense of fat deposition.

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Biological Activity

Bioactivity / Mechanism

In a mouse study of the β2-adrenergic agonist clenbuterol, the hydrochloride produced transient, muscle-type-dependent signaling responses. A single 1.0 mg/kg injection increased p38 MAPK and Akt phosphorylation in soleus at 1 and 4 h, while tibialis anterior changes were not statistically significant. CREB phosphorylation was reported unchanged. These downstream observations do not by themselves establish receptor dependence or muscle hypertrophy. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

In Vitro Studies

Clenbuterol hydrochloride altered lymphocyte proliferation in cultured equine PBMCs in a concentration- and donor-dependent pattern. At 0.6 ng/mL, proliferation increased in total, CD4+ and CD8+ lymphocytes from untrained horses; higher tested concentrations did not reproduce this effect. In well-trained donors, only total lymphocyte proliferation increased at 1.6 ng/mL. These findings apply to the study’s stimulated culture system; they do not demonstrate an in-vivo effect. [2]

Concentration- and donor-dependent lymphocyte proliferation ex vivo

Cell-based study · PBMCs from 28 thoroughbred horses sampled after acute exercise: 14 untrained and 14 well-trained donors; cells treated in vitro [2]

CellTrace dilution indicated increased total, CD4+ and CD8+ lymphocyte proliferation at 0.6 ng/mL in untrained donors, but not at 1.0 or 1.6 ng/mL. In well-trained donors, only total lymphocyte proliferation increased at 1.6 ng/mL; CD4+ and CD8+ proliferation did not change significantly. No in-vivo clenbuterol intervention was performed.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Proliferation of total, CD4+ and CD8+ lymphocytes	Reciprocal CellTrace Violet MFI (1/MFI) Untrained: increase versus untreated cells at 0.6 ng/mL in all three populations (P < 0.05); no detected effect at 1.0 or 1.6 ng/mL. Well-trained: total lymphocytes increased at 1.6 ng/mL (P < 0.05); no detected CD4+/CD8+ effect.	[2]

Literature-Reported Treatment Conditions

Treatment concentration: 0.6, 1.0 and 1.6 ng/mL
Exposure duration: Four-day PBMC culture
Method: In-vitro exposure of donor-matched PBMC cultures; CellTrace Violet flow-cytometric proliferation readout
Vehicle: PBS stock diluted into RPMI 1640 with GlutaMAX; same-horse control cultures without CLEN
Co-treatment: Shared Methods 2.3 describe cultures with or without PHA, followed after 24 h by washing and IL-2 for three further days. Figure 1 does not label separate stimulation strata; effects are restricted to the reported culture system.
Reported limits: Exact PHA stratum for Figure 1 and final PBS fraction are not specified in the figure-specific reporting. Do not attribute these results to clenbuterol alone in unstimulated cells. Donor age differs with training status; training causality is not isolated.

Methods and source locations

Compound reported in the paper: Clenbuterol hydrochloride; Compound label in the paper: CLEN

Salt-matched cellular observations under the reported culture conditions; no equine dosing recommendation or in-vivo immune-efficacy claim.

Methods 2.1–2.5, 2.7; Results 3.1; Figure 1A–H and caption; Limitations 4.4

Proliferation of total, CD4+ and CD8+ lymphocytes: Flow cytometry after reported four-day culture. No exact response magnitudes inferred from scatter plots. Figure caption: means ± SEM, n = 28 overall; Methods: 14 donors in each fitness group; groups analyzed separately by one-way ANOVA/Tukey HSD. — Results 3.1; Figure 1A–H and caption; Methods 2.1, 2.4–2.5, 2.7

In Vivo Studies

An adverse outcome was reported in a mouse stroke model using material identified as Adooq A13407. Intraperitoneal clenbuterol at 1 mg/kg, given 24 and 48 h after MCAO, increased TTC-defined infarct burden at 72 h from 35.0 ± 7.1% with saline to 45.8 ± 6.4% (mean ± SEM; n = 6 per group; P < 0.05). The mechanism of the larger infarct was not established. [3]

Acute muscle-type-dependent phosphorylation in mice

Animal study · Male 10-week-old C57BL/6J mice; soleus and tibialis anterior (TA) muscles [1]

A single treatment increased normalized p38 MAPK and Akt phosphorylation in soleus at 1 and 4 h. TA responses were not statistically significant. No change in CREB phosphorylation was reported at 1–24 h (data not shown). The experiment measures acute signaling, without establishing that these changes cause hypertrophy or are directly receptor-mediated.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Phosphorylated p38 MAPK normalized to total p38; control optical density set to 1	Relative phosphorylation Soleus: 580% at 1 h and 460% at 4 h; both significant. TA: 170% (P = 0.14) and 160% (P = 0.19), respectively. Mean ± SEM; n = 4.	[1]
Phosphorylated Akt (Ser473) normalized to total Akt	Relative phosphorylation Soleus: 360% at 1 h and 240% at 4 h, significant; TA: no significant change. Mean ± SEM; n = 4.	[1]
CREB phosphorylation in soleus and TA	Reported null result No change at 1–24 h after single-dose treatment; data not shown.	[1]

Conditions shared by the study groups

Route: Intraperitoneal
Frequency: Once
Treatment course: Endpoints at 1, 4 and 24 h
Vehicle: 0.9% NaCl

Study groups and reported outcomes
Group / dose	Comparator	Observed result	Reference
Single-dose clenbuterol 1.0 mg/kg body weight	Control mice (normalization = 1); acute control injection details not specified	Transient significant soleus p38/Akt phosphorylation at 1 and 4 h; TA changes not significant.	[1]

Single-dose clenbuterol: Model: Male C57BL/6J mice; soleus and TA; Reported limits: No acute vehicle-only injection explicitly specified in methods.

Methods and source locations

Compound reported in the paper: Clenbuterol hydrochloride; Compound label in the paper: clenbuterol

Salt-matched literature on mouse signaling; not a potency or current-product quality claim.

Materials and methods: Experimental animals, Acute experiment, Western blotting analysis, Statistical analysis; Results; Figures 1a and 2a with captions

Phosphorylated p38 MAPK normalized to total p38; control optical density set to 1: Western blot; actin loading control; percentages are reported in Results, not estimated from bars. — Results p38 paragraph; Figure 1a and caption

Phosphorylated Akt (Ser473) normalized to total Akt: Western blot; actin loading control; values from Results. Figure 2a marks soleus 1 h ***P < 0.001 and 4 h **P < 0.01 versus control. — Results Akt paragraph; Figure 2a and caption

CREB phosphorylation in soleus and TA: Phospho-CREB (Ser133) immunoblot described in shared methods; underlying image not supplied in the article. — Results opening paragraph; Western blotting analysis for β2-AR signaling molecules

Single-dose clenbuterol · Materials and methods: Experimental animals, Acute experiment, Western blotting analysis, Statistical analysis; Results; Figures 1a and 2a with captions

Larger infarct burden after post-stroke clenbuterol treatment

Animal study · Male C57BL/6 mice, 8–10 weeks old; transient MCAO with reperfusion [3]

Compared with saline-treated MCAO mice, clenbuterol-treated mice had greater TTC-defined infarct burden at 72 h. The authors did not characterize the mechanism of this adverse effect.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
TTC-defined infarct burden, expressed as percentage; paper calls this infarct volume	Infarct size (%) M-saline: 35.0 ± 7.1%; M-CLEN: 45.8 ± 6.4%; P < 0.05; n = 6 per group; mean ± SEM per shared statistics.	[3]

Conditions shared by the study groups

Route: Intraperitoneal
Frequency: At 24 h and 48 h after MCAO
Treatment course: Two administrations; TTC endpoint 72 h after MCAO
Vehicle: 0.9% sodium chloride

Study groups and reported outcomes
Group / dose	Comparator	Observed result	Reference
MCAO plus CLEN 1 mg/kg	M-saline: MCAO mice receiving saline; n = 6 per infarct comparison group	Infarct burden 45.8 ± 6.4% versus 35.0 ± 7.1% with saline (P < 0.05).	[3]

MCAO plus CLEN: Model: Male 8–10-week-old C57BL/6 mice after MCAO; Reported limits: Administration volume not provided; retain additional 0.1 mM wording privately without conversion.

Methods and source locations

Compound reported in the paper: Clenbuterol hydrochloride; Compound label in the paper: CLEN (Adooq Bioscience A13407)

Reported adverse result for named A13407 material in this mouse model; not generalized neuroprotection or therapeutic guidance.

Methods: Stroke Model and Drug Treatment, Assessment of Infarct Volume, Statistical Analysis; Results first subsection; Figure 1A–C and caption; Limits

TTC-defined infarct burden, expressed as percentage; paper calls this infarct volume: TTC-stained coronal sections; infarct areas and total slice area measured by Image-Pro Plus. Numeric values from Results, supported visually by Figure 1C. Caption names one-way ANOVA with post-hoc; general methods describe Holm–Sidak correction for three-group comparisons. — Results first subsection, infarct comparison; Figure 1B–C and caption; Assessment of Infarct Volume; Statistical Analysis

MCAO plus CLEN · Methods: Stroke Model and Drug Treatment, Assessment of Infarct Volume, Statistical Analysis; Results first subsection; Figure 1A–C and caption; Limits

Specifications

Manufacturer	Adooq Bioscience
Actions	Agonist
CAS Number	21898-19-1
Formula	C₁₂H₁₈Cl₂N₂O.HCl
Molecular Weight	313.65
SMILES	CC(C)(C)NCC(C1=CC(=C(C(=C1)Cl)N)Cl)O.Cl

Storage & Solubility

In Vitro Solubility

Reported Solubility

No reported solubility data are available for this product.

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

[1] Shogo Sato, Ken Shirato, Ryosuke Mitsuhashi, et al. Intracellular β2-adrenergic receptor signaling specificity in mouse skeletal muscle in response to single-dose β2-agonist clenbuterol treatment and acute exercise The journal of physiological sciences : JPS (2013). PMID: 23508836 DOI: 10.1007/s12576-013-0253-z Source material
[2] Olga Witkowska-Piłaszewicz, Rafał Pingwara, Jarosław Szczepaniak, et al. The Effect of the Clenbuterol-β2-Adrenergic Receptor Agonist on the Peripheral Blood Mononuclear Cells Proliferation, Phenotype, Functions, and Reactive Oxygen Species Production in Race Horses In Vitro Cells (2021). PMID: 33920705 DOI: 10.3390/cells10040936 Source material
[3] Younian Xu, Yangyang Ge, Miaomiao Zhou, et al. Clenbuterol, a Selective β2-Adrenergic Receptor Agonist, Inhibits or Limits Post-Stroke Pneumonia, but Increases Infarct Volume in MCAO Mice Journal of inflammation research (2022). PMID: 35058704 DOI: 10.2147/jir.s344521 Source material

Publications

1 publication citing this product

Younian Xu, .et al. , J Inflamm Res, 2022, Jan 14;15:295-309 PMID: 35058704

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Clenbuterol hydrochloride

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