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Fig. 1 · Structure
Cat. No.
A11271
CAS No.
22862-76-6
Formula
C14H19NO4
Mol. Weight
265.31

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Anisomycin

Cat. No. A11271 CAS 22862-76-6

SAPKs/JNKs activator

Anisomycin is a pyrrolidine antibiotic, acts as an anti-fungal antibiotic which inhibits Protein Synthesis, also is a potent activator of SAPKs/JNKs.

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Publications for Anisomycin

2 publications citing this product

  1. Ken Kobayashi, .et al. , Cell Tissue Res, 2022, Sep;389(3):501-515 PMID: 35748981
  2. Li Li, .et al. , Cancer Cell Int, 2021, May 13;21(1):260 PMID: 33985519
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For laboratory research use only. We do not sell to patients.

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Biological Activity

Bioactivity / Mechanism

Anisomycin is used to perturb translation-associated ribosome stress signaling. In HEK293 cells, intermediate exposure increased RNase-resistant disomes and p38/JNK phosphorylation more strongly than high exposure. In MCF10A cells, ZAK deletion prevented the p38 response; re-expression of ZAKα restored it, whereas ZAKβ or kinase-defective ZAKα-K45M did not. These experiments support ribosome-linked signaling through ZAKα in the tested models. [1]

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

Target & Activity

Target Activity Value
JNK

Cellular Effect

Cell Line Activity Value Description Reference
Vero C1008 CC50 < 0.39 μM CC50 determination at MOI 0.004 using CellTiter- Glo (CTG) assay, performed 3 days post-infection in Vero E6 cells 10.1101/2020.03.25.008482
Vero C1008 CC50 < 0.39 μM CC50 determination at MOI 0.01 using CellTiter- Glo (CTG) assay, performed 3 days post-infection in Vero E6 cells 10.1101/2020.03.25.008482

In Vitro Studies

Anisomycin-induced stress-kinase phosphorylation depends on model and exposure conditions. The acute HEK293 response was strongest at intermediate concentrations, while a separate U2OS experiment detected p38/JNK phosphorylation at both low and high exposure after 1 h. The HEK293 pattern should therefore not be treated as a universal concentration-response rule. [1,2]

Concentration-dependent ribosome stress and p38/JNK phosphorylation

Cell-based study · HEK293 (Flp-In T-REx 293) cells [1]

Intermediate anisomycin exposure produced more RNase-resistant disomes and stronger p38/JNK phosphorylation than high exposure. Emetine pretreatment prevented the anisomycin p38 response. These are cellular ribosome-stress and phosphorylation endpoints, not a direct kinase-binding assay.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
RNase-resistant disome accumulationqualitative comparison Greater at 1 mg/L than at 100 mg/L or untreated[1]
p38/JNK phosphorylation and emetine pretreatment controlqualitative immunoblot result Strongest at intermediate rather than high anisomycin concentrations; p38 response prevented by high-dose emetine pretreatment[1]

Literature-Reported Treatment Conditions

Treatment concentration
Figure 1B: 0, 1 or 100 mg/L; Figure 1C: 0.001–100 mg/L. Figure 1E: anisomycin 1 mg/L; emetine pretreatment 48 mg/L.
Exposure duration
Figure 1C and 1E: anisomycin 15 min; Figure 1E emetine pretreatment 5 min. Figure 1B-specific exposure duration is not stated in its caption.
Method
RNase-digested polysome profiles and phospho-p38/phospho-JNK immunoblots; untreated controls and total p38 loading control.
Vehicle
Ethanol used for anisomycin stock; final ethanol fraction not stated for these panels.
Co-treatment
Figure 1E is emetine pretreatment plus anisomycin; Figures 1B/C are anisomycin exposures.
Reported limits
No fitted potency, numerical fold-change or per-panel exact replicate count supplied for these blots. Methods state representative blots from at least two independent experiments. Do not transfer timing from the immunoblot to Figure 1B.
Methods and source locations

Compound reported in the paper: Anisomycin; Compound label in the paper: ANS

Reported anisomycin experiments; no salt conversion, stereochemical assay or current Adooq lot equivalence established.

Results: Ribosome collisions activate SAPKs; Figure 1B, 1C, 1E and captions; STAR Methods: Immunoblot analysis, Antibodies, polysome profiling.

RNase-resistant disome accumulation: RNase-digested polysome profiles; no peak areas digitized. — Figure 1B and Results: Ribosome collisions activate SAPKs

p38/JNK phosphorylation and emetine pretreatment control: Phospho-specific immunoblots with total p38; representative blots from at least two independent experiments per shared methods. — Figure 1C, 1E and captions

ZAK isoform and kinase-activity validation of the p38 response

Cell-based study · MCF10A wild-type, ZAK-knockout, and knockout cells complemented with ZAKα, ZAKα-K45M or ZAKβ [1]

Anisomycin-induced p38 phosphorylation was lost after ZAK deletion and restored by ZAKα, while ZAKβ and ATP-binding-defective ZAKα-K45M failed to restore the response.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
ZAK dependence and isoform specificity of phospho-p38 responsequalitative genetic rescue ZAKα restored the response; ZAKβ and ZAKα-K45M did not[1]

Literature-Reported Treatment Conditions

Treatment concentration
1 mg/L
Exposure duration
15 min
Method
Phospho-p38 immunoblot; matched untreated genotypes, total p38 and ZAK isoform expression blots.
Vehicle
Ethanol stock; final fraction not specified.
Co-treatment
Genetic complementation; no second pharmacological treatment adopted.
Reported limits
Per-panel exact n and quantitative rescue magnitude not provided. Shared immunoblot methods state at least two independent experiments.
Methods and source locations

Compound reported in the paper: Anisomycin; Compound label in the paper: ANS

Reported anisomycin experiments; no salt conversion, stereochemical assay or current Adooq lot equivalence established.

Results: ZAK is required for ribosome collision-induced SAPK activation; Figure 2A and caption; STAR Methods: cell lines, Immunoblot analysis, Antibodies.

ZAK dependence and isoform specificity of phospho-p38 response: Phospho-p38/total p38 and ZAKα/ZAKβ immunoblots with untreated and treated genotype controls. — Figure 2A, lanes 1–10 and caption

Sustained U2OS response at low and high anisomycin exposure

Cell-based study · U2OS human osteosarcoma cells [2]

In U2OS cells, both low and high anisomycin treatment produced p38 and JNK phosphorylation after 1 h. This limits extrapolation of the HEK293 concentration-response pattern to other cell models or exposure times.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
p38/JNK phosphorylation after low and high anisomycin treatmentqualitative immunoblot comparison Detectable at both ani L and ani H after 1 h in U2OS[2]

Literature-Reported Treatment Conditions

Treatment concentration
Ani L: 0.19 μM; ani H: 76 μM (L/H definitions in Results and Figure 5A caption; applied as ani L/H in Figure 5E).
Exposure duration
1 h
Method
Figure 5E anisomycin lanes compared with untreated lane; phospho-p38, total p38, phospho-JNK, total JNK and γ-tubulin immunoblots.
Vehicle
Vehicle composition is not specified for Figure 5E in the retrieved caption/materials; do not transfer the DMSO control of the separate ribosome-profiling experiment.
Co-treatment
Anisomycin-only lanes adopted. The harringtonine lane is not adopted.
Reported limits
No fitted EC50, quantitative band ratio or exact Figure 5E biological replicate count reported in the read locations.
Methods and source locations

Compound reported in the paper: Anisomycin; Compound label in the paper: ANS

Reported anisomycin experiments; no salt conversion, stereochemical assay or current Adooq lot equivalence established.

Results paragraph beginning We treated U2OS cells with L and H concentrations; Figure 5E and caption, with L/H definitions in Figure 5A; Methods: Cell culture, Western blot and immunoprecipitation.

p38/JNK phosphorylation after low and high anisomycin treatment: Phospho and total kinase blots with γ-tubulin; no numerical fold-change inferred. — Figure 5E anisomycin lanes, Results L/H definitions and Figure 5 caption

In Vivo Studies

In male rats, bilateral ventral-hippocampal anisomycin before training reduced inhibitory-avoidance retention latency 48 h later. A separate microdialysis design found transient increases in local norepinephrine and dopamine release. These findings support its use as an experimental perturbation while limiting attribution of the behavioral effect solely to blocked protein synthesis. [3]

Pretraining hippocampal anisomycin and 48-hour avoidance retention

Animal study · Male Sprague-Dawley rats, approximately 3 months old; anisomycin N = 5, aCSF N = 6 [3]

Pretraining anisomycin reduced retention latency at the 48-hour inhibitory-avoidance memory test relative to aCSF. The endpoint is behavioral retention, without establishing that protein-synthesis inhibition alone caused the deficit.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Latency to enter the shock compartment at the 48-h retention testbetween-group Mann–Whitney U-test Lower with anisomycin than aCSF; P < 0.005; ANI N = 5, aCSF N = 6[3]

Conditions shared by the study groups

Route
Bilateral infusion into ventral hippocampus
Frequency
Single infusion per side
Treatment course
20 min before training; test at 48 h
Vehicle
Artificial cerebrospinal fluid (aCSF); solution adjusted to pH 7.2.
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Anisomycin versus aCSF
125 μg per side in 1 μL		aCSF N = 6; anisomycin N = 5Lower retention latency after anisomycin; P < 0.005[3]
Anisomycin versus aCSF
Model: Male Sprague-Dawley rats, approximately 3 months old
Reported limits: Anisomycin lot purity and stereochemical characterization not reported in the retrieved methods.
Methods and source locations

Compound reported in the paper: Anisomycin; Compound label in the paper: ANI

Reported anisomycin experiments; no salt conversion, stereochemical assay or current Adooq lot equivalence established.

Results: Pretraining administration of anisomycin into the hippocampus impaired memory; Figure 1 and caption; Methods: Subjects, Injections and microdialysis procedures, Inhibitory avoidance training and memory testing, Histology, Statistics.

Latency to enter the shock compartment at the 48-h retention test: Retention latency; plotted median ± interquartile range; no exact seconds transcribed. — Figure 1; Results first subsection; Methods: Statistics

Anisomycin versus aCSF · Figure 1; Methods: Injections and microdialysis procedures; Inhibitory avoidance training and memory testing

Hippocampal norepinephrine and dopamine release after anisomycin

Animal study · Male Sprague-Dawley rats, approximately 3 months old; NE/DA cohort: anisomycin N = 5, aCSF N = 6 [3]

Anisomycin transiently increased hippocampal norepinephrine and dopamine release during the first post-infusion sample. Values returned toward baseline in later samples, showing that local administration alters neurotransmission as well as behavioral retention.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Norepinephrine release in the first 60-min post-infusion samplepercent of baseline 731% of baseline (Results); ANI N = 5, aCSF N = 6[3]
Dopamine release in the first 60-min post-infusion samplepercent of baseline 544% of baseline (Results); ANI N = 5, aCSF N = 6[3]

Conditions shared by the study groups

Route
Bilateral infusion into ventral hippocampus
Frequency
Single infusion per side
Treatment course
Single infusion; 2 h baseline and 3 h post-infusion sampling
Vehicle
Artificial cerebrospinal fluid (aCSF); solution adjusted to pH 7.2.
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Anisomycin versus aCSF
125 μg per side in 1 μL		aCSF N = 6; anisomycin N = 5Transient first-sample rise in NE and DA; no sustained elevation claimed[3]
Anisomycin versus aCSF
Model: Male Sprague-Dawley rats; NE/DA microdialysis cohort
Reported limits: Anisomycin lot purity and stereochemical characterization not reported in the retrieved methods.
Methods and source locations

Compound reported in the paper: Anisomycin; Compound label in the paper: ANI

Reported anisomycin experiments; no salt conversion, stereochemical assay or current Adooq lot equivalence established.

Results: Anisomycin produced large increases in NE, DA, and ACh release, NE/DA paragraphs only; Figures 2–3 and captions; Methods: Subjects, Injections and microdialysis procedures, NE and DA assay procedures, Statistics.

Norepinephrine release in the first 60-min post-infusion sample: HPLC-ED following microdialysis; figure shows mean ± S.E.M.; no additional precision inferred. — Results NE paragraph; Figure 2 and caption; Methods: Injections and microdialysis procedures

Dopamine release in the first 60-min post-infusion sample: HPLC-ED following microdialysis; figure shows mean ± S.E.M.; later samples reported not different from baseline (Ps > 0.2). — Results DA paragraph; Figure 3 and caption; Methods: Injections and microdialysis procedures

Anisomycin versus aCSF · Figures 2–3 and Results NE/DA paragraphs; Methods: Injections and microdialysis procedures

Specifications

Manufacturer Adooq Bioscience
Actions Activator
CAS Number 22862-76-6
Applications SAPKs/JNKs activator
Formula C14H19NO4
Molecular Weight 265.31
Synonyms Flagecidin; Wuningmeisu C
SMILES
O[C@@H]1[C@H]([C@@H](CC(C=C2)=CC=C2OC)NC1)OC(C)=O

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO Warmed: 35 mg/mL (131.92 mM)
Water Insoluble
Ethanol Warmed: 14 mg/mL (52.76 mM)

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.

In Vivo Preparation

Concentration
4 mg/mL
Vehicle
2% DMSO+corn oil

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. [1] Colin Chih-Chien Wu, Amy Peterson, Boris Zinshteyn, et al. Ribosome Collisions Trigger General Stress Responses to Regulate Cell Fate Cell (2020). PMID: 32610081 DOI: 10.1016/j.cell.2020.06.006 Source material
  2. [2] Anna Constance Vind, José Francisco Martínez, Zhenzhen Wu, et al. Mechanism of RACK1-dependent ZAKα activation at stalled and collided ribosomes Molecular Cell (2026). PMID: 42214329 DOI: 10.1016/j.molcel.2026.04.034 Source material
  3. [3] Zhenghan Qi, Paul E Gold. Intrahippocampal infusions of anisomycin produce amnesia: contribution of increased release of norepinephrine, dopamine, and acetylcholine Learning & Memory (2009). PMID: 19403793 DOI: 10.1101/lm.1333409 Source material

Publications

2 publications citing this product

  1. Ken Kobayashi, .et al. , Cell Tissue Res, 2022, Sep;389(3):501-515 PMID: 35748981
  2. Li Li, .et al. , Cancer Cell Int, 2021, May 13;21(1):260 PMID: 33985519

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