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Fig. 1 · Structure
Cat. No.
A10503
CAS No.
525-79-1
Formula
C10H9N5O
Mol. Weight
215.2

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Kinetin

Cat. No. A10503 CAS 525-79-1
Kinetin is a kind of cytokinin, a class of plant hormone that promotes cell division.

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Publications for Kinetin

1 publication citing this product

  1. Sadaf Javed, .et al. , J Exp Molec Biol, 2024, 25(2)
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Biological Activity

Bioactivity / Mechanism

Kinetin restored ubiquitin phosphorylation in cells expressing engineered human PINK1 M318G when combined with mitochondrial depolarization. This chemical-genetic result concerns a modified gatekeeper mutant and does not establish direct activation of native PINK1. [1]

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

In Vitro Studies

In the engineered PINK1 M318G cell model, 200 μM kinetin was active with oligomycin/antimycin A cotreatment. Extending kinetin exposure from 2 to 24 hours did not improve phospho-ubiquitin output and impaired cell growth and/or survival. [1]

Kinetin response in engineered PINK1 M318G cells

Cell-based study · HeLa PINK1−/− YFP-Parkin cells expressing human PINK1 M318G, transiently or stably [1]

Kinetin plus mitochondrial depolarization restored ubiquitin phosphorylation in this engineered gatekeeper-mutant system; adenine did not substitute. Longer exposure did not improve the response and impaired growth and/or survival.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Ubiquitin Ser65 phosphorylation; PINK1 and Parkin phosphorylationqualitative immunoblot response Kinetin + OA increased phosphorylation relative to OA alone; adenine + OA did not restore the M318G response. Experiments performed in triplicate.[1]
Response to extending kinetin exposurequalitative limitation 24 h did not increase phospho-ubiquitin and hampered cell growth and/or survival.[1]

Literature-Reported Treatment Conditions

Treatment concentration
200 μM kinetin; 200 μM adenine comparator
Exposure duration
2 h; an additional 24 h kinetin condition was assessed in transiently expressing cells
Method
Cell treatment followed by immunoblotting and Phos-tag analysis
Co-treatment
10 μM oligomycin plus 4 μM antimycin A (OA), added for the final 2 h; includes OA-alone and non-OA controls
Reported limits
Kinetin solvent, vendor and purity are not specified in the acquired cell-treatment methods.
Methods and source locations

Compound reported in the paper: Kinetin; Compound label in the paper: kinetin

Applies to reported kinetin material and stated model; no Adooq lot, purity, or formulation equivalence was established.

Fig. 4A–C and caption; Results: Kinetin activates human PINK1 gatekeeper mutants in cells; Methods: Transient transfection and Western blotting

Ubiquitin Ser65 phosphorylation; PINK1 and Parkin phosphorylation: Immunoblot and Phos-tag; GAPDH loading control — Fig. 4A–C and caption; Results: Kinetin activates human PINK1 gatekeeper mutants in cells; Methods: Transient transfection and Western blotting

Response to extending kinetin exposure: Authors’ interpretation of Fig. 4B; not a quantitative viability assay — Fig. 4A–C and caption; Results: Kinetin activates human PINK1 gatekeeper mutants in cells; Methods: Transient transfection and Western blotting

In Vivo Studies

Chronic dietary kinetin increased ELP1 exon 20 inclusion and protein in peripheral ganglia of familial-dysautonomia mice. The response varied by tissue: cortical endpoints were not significantly changed, and heart protein did not increase significantly. [2]

In male Thy1-hSyn transgenic mice, long-term dietary kinetin did not improve open-field hyperactivity and worsened balance-beam foot slips and traversal time. These findings limit extrapolation from cellular PINK1-pathway responses to behavioral benefit. [3]

In aged male C57BL/6J mice, six weeks of dietary kinetin reduced liver minor-arc mitochondrial-DNA deletion frequency relative to same-age controls. This molecular endpoint does not establish behavioral benefit or direct PINK1 target engagement. [4]

Tissue-specific ELP1 response in familial-dysautonomia mice

Animal study · TgFD9;IkbkapΔ20/flox phenotypic FD mice (C57BL/6J background), assessed at 6 months [2]

Chronic dietary kinetin increased exon 20 inclusion and ELP1 protein in peripheral ganglia and several organs. Cortical endpoints and heart protein did not show significant improvement.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Exon 20 inclusion in dorsal root ganglia and ELP1 protein in trigeminal gangliabetween-group significance Exon inclusion: p < 0.001; ELP1 protein: p < 0.01. Vehicle n = 13–14; kinetin n = 13. Means and SEM; individual points are animals.[2]
Cortical exon inclusion/protein and heart ELP1 proteinnon-significant results Cortex exon inclusion p = 0.24; cortex protein p = 0.39; heart protein p = 0.06. Heart exon inclusion increased (p < 0.001).[2]

Conditions shared by the study groups

Route
Oral diet; exposure through treated dams before weaning
Frequency
Ad libitum diet
Treatment course
P0 to 6 months
Vehicle
LabDiet 5P00
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Kinetin diet versus control diet
2150 ppm kinetin chow, formulated to provide 200 mg/kg/day		Vehicle-fed FD micePeripheral ganglia showed higher exon inclusion and ELP1 protein; cortex did not. Lung, liver and kidney showed increases in both endpoints.[2]
Kinetin diet versus control diet
Model: TgFD9;IkbkapΔ20/flox FD mice
Reported limits: Individual consumed dose and preweaning milk exposure were not quantified for this adopted endpoint.
Methods and source locations

Compound reported in the paper: Kinetin; Compound label in the paper: kinetin

Applies to reported kinetin material and stated model; no Adooq lot, purity, or formulation equivalence was established.

Fig. 3A–F and caption; Study Design; RNA Isolation and RT-PCR Analysis; Meso-Scale Discovery Immunoassay

Exon 20 inclusion in dorsal root ganglia and ELP1 protein in trigeminal ganglia: Human-specific RT-PCR and MSD immunoassay; two-tailed unpaired Student’s t test — Fig. 3A–F and caption; Study Design; RNA Isolation and RT-PCR Analysis; Meso-Scale Discovery Immunoassay

Cortical exon inclusion/protein and heart ELP1 protein: RT-PCR and MSD; two-tailed unpaired Student’s t test — Fig. 3A–F and caption; Study Design; RNA Isolation and RT-PCR Analysis; Meso-Scale Discovery Immunoassay

Kinetin diet versus control diet · Fig. 3A–F and caption; Study Design; RNA Isolation and RT-PCR Analysis; Meso-Scale Discovery Immunoassay

Negative behavioral findings in α-synuclein transgenic mice

Animal study · Male Thy1-hSyn line 61 mice and wild-type controls, tested at 6 months [3]

Dietary kinetin did not improve open-field hyperactivity. In transgenic mice, it increased balance-beam foot slips and traversal time; the increase in falls was not significant.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Open-field ambulations and rearingschow main-effect p values Ambulations p = 0.42; rearings p = 0.99. n = 10 WT standard, 10 WT kinetin, 12 Syn standard, 8 Syn kinetin; mean ± SE.[3]
Balance-beam foot slips, falls and traversal timedirection and chow main-effect p values Foot slips increased (chow p = 0.0034); traversal time increased (chow p = 0.0031); falls increase not significant (chow p = 0.13). n = 10 WT standard, 10 WT kinetin, 9 Syn standard, 8 Syn kinetin; mean ± SE.[3]

Conditions shared by the study groups

Route
Oral chow
Frequency
Ad libitum
Treatment course
From weaning through behavioral testing at 6 months (Fig. 5 reports 4.5 months)
Vehicle
Purina 5053
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Kinetin diet with WT and transgenic controls
3.50 g kinetin/kg chow; reported average 400 mg/kg body weight/day		Standard-chow WT and Thy1-hSyn groups; WT kinetin groupNo improvement of hyperactivity; adverse balance-beam performance in Thy1-hSyn mice.[3]
Kinetin diet with WT and transgenic controls
Model: Male Thy1-hSyn line 61 and WT mice
Reported limits: Actual individual intake was not a fixed gavage dose; direct PINK1 engagement unconfirmed.
Methods and source locations

Compound reported in the paper: Kinetin; Compound label in the paper: kinetin

Applies to reported kinetin material and stated model; no Adooq lot, purity, or formulation equivalence was established.

Fig. 5A–F and caption; sections 2.1–2.2, 2.11–2.12 and 3.5

Open-field ambulations and rearings: Two-way ANOVA with Bonferroni post-test — Fig. 5A–F and caption; sections 2.1–2.2, 2.11–2.12 and 3.5

Balance-beam foot slips, falls and traversal time: Two-way ANOVA with Bonferroni post-test; group direction from Results and Fig. 5, not inferred from main-effect p alone — Fig. 5A–F and caption; sections 2.1–2.2, 2.11–2.12 and 3.5

Kinetin diet with WT and transgenic controls · Fig. 5A–F and caption; sections 2.1–2.2, 2.11–2.12 and 3.5

Liver mitochondrial-DNA deletion endpoint in aged mice

Animal study · Male C57BL/6J mice, 16.5 months old at treatment start [4]

Six weeks of dietary kinetin reduced a naturally accumulating liver mtDNA deletion relative to same-age controls. This endpoint does not demonstrate behavioral improvement or direct PINK1 engagement.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Liver minor-arc mitochondrial-DNA deletion frequencyreported fold reduction versus same-age control chow 10-fold reduction after 6 weeks (Fig. 4G caption); figure marks p < 0.001. Error bars: standard error.[4]

Conditions shared by the study groups

Route
Oral diet
Frequency
Ad libitum
Treatment course
6 weeks; assessed at 18 months
Vehicle
Purina 5053 chow
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Aged mice: kinetin chow versus control chow
3.50 g kinetin/kg chow		Same-age mice given control chowReduced liver minor-arc mtDNA deletion frequency[4]
Aged mice: kinetin chow versus control chow
Model: Male C57BL/6J mice, 16.5 months old at treatment start
Reported limits: Body-weight-normalized dose and Fig. 4G animal count are not specified in the acquired caption/regimen. Two liver fragments were analyzed per animal; do not equate fragments with independent animals.
Methods and source locations

Compound reported in the paper: Kinetin; Compound label in the paper: kinetin

Reported parent kinetin material; no Adooq lot equivalence or human efficacy established.

Fig. 4E–G and caption; Results: aged-mouse minor-arc deletion experiment; Methods: Mice; Kinetin Chow; DNA Isolation; ddPCR Analyses

Liver minor-arc mitochondrial-DNA deletion frequency: Droplet digital PCR using deletion-specific and common mtDNA assays; one-way ANOVA/Tukey multiple comparisons as stated in caption — Fig. 4E–G and caption; Results: aged-mouse minor-arc deletion experiment; Methods: Mice; Kinetin Chow; DNA Isolation; ddPCR Analyses

Aged mice: kinetin chow versus control chow · Fig. 4E–G and caption; Results: aged-mouse minor-arc deletion experiment; Methods: Mice; Kinetin Chow; DNA Isolation; ddPCR Analyses

Specifications

Manufacturer Adooq Bioscience
CAS Number 525-79-1
Formula C10H9N5O
Molecular Weight 215.2
Synonyms 6-Furfuryladenine; N6-Furfuryladenine; 6-Furfurylaminopurine; Cytokinin
SMILES
C1=COC(=C1)CNC2=NC=NC3=C2NC=N3

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO Warmed: 8 mg/mL (37.17 mM)
Water Insoluble
Ethanol Insoluble

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. [1] Zhong Yan Gan, Sylvie Callegari, Thanh N Nguyen, et al. Interaction of PINK1 with nucleotides and kinetin Science Advances (2024). PMID: 38241364 DOI: 10.1126/sciadv.adj7408 Source material
  2. [2] Elisabetta Morini, Dadi Gao, Connor M Montgomery, et al. ELP1 Splicing Correction Reverses Proprioceptive Sensory Loss in Familial Dysautonomia American Journal of Human Genetics (2019). PMID: 30905397 DOI: 10.1016/j.ajhg.2019.02.009 Source material
  3. [3] Adam L Orr, Florentine U Rutaganira, Daniel de Roulet, et al. Long-term oral kinetin does not protect against α-synuclein-induced neurodegeneration in rodent models of Parkinson's disease Neurochemistry international (2017). PMID: 28434973 DOI: 10.1016/j.neuint.2017.04.006 Source material
  4. [4] Pei-I Tsai, Ekaterina Korotkevich, Patrick H O’Farrell. Mitigation of age-dependent accumulation of defective mitochondrial genomes Proceedings of the National Academy of Sciences of the United States of America (2022). PMID: 35881807 DOI: 10.1073/pnas.2119009119 Source material

Publications

1 publication citing this product

  1. Sadaf Javed, .et al. , J Exp Molec Biol, 2024, 25(2)

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