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Kinetin (N6-Furfuryladenine)

Alias: 6-Furfuryladenine; NSC23119; NSC 23119; NSC-23119; Kinetin
Cat No.:V1993 Purity: ≥98%
Kinetin (also called 6-Furfuryladenine; N6-Furfuryladenine) is a cytokinin compound and a class of plant hormone that promotes cell division.
Kinetin (N6-Furfuryladenine)
Kinetin (N6-Furfuryladenine) Chemical Structure CAS No.: 525-79-1
Product category: Plants
This product is for research use only, not for human use. We do not sell to patients.
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Purity & Quality Control Documentation

Purity: ≥98%

Product Description

Kinetin (also called 6-Furfuryladenine; N6-Furfuryladenine) is a cytokinin compound and a class of plant hormone that promotes cell division. Kinetin is often used in plant tissue culture for inducing formation of callus (in conjunction with auxin) and to regenerate shoot tissues from callus. At present, kinetin is one of the widely used anti-aging agents in numerous skin care cosmetics and cosmeceuticals, such as Valeant products kinerase.

Biological Activity I Assay Protocols (From Reference)
Targets
Kinetin (N6-Furfuryladenine) modulates platelet free radical generation and aggregation-related pathways [1]
Kinetin (N6-Furfuryladenine) regulates IKBKAP gene pre-mRNA splicing [2][3]
Kinetin riboside (derivative of Kinetin) targets tumor cell proliferation-related pathways [4]
ln Vitro
Kinetin (N6-furfuryladenine) slows the development and aging of insects, delays the onset of many age-related characteristics seen in normal human skin fibroblasts aged in vitro, and has a direct effect on superoxide dismutase activity in plants. It also prevents the oxidation of unsaturated acids in plant membranes, reduces insect fecundity, and increases the specific activity of catalase. The production of hydroxyl radicals is greatly inhibited by kinetin (70-150 μM) by roughly 41% and 76%, respectively [1]. The cytokinin kinetin found in plants considerably raises the quantity of exon 20 in RNA extracted from cultivated familial dysautonomia (FD) cells [2].
Kinetin (N6-Furfuryladenine) (10-100 μM) dose-dependently inhibited free radical formation in ADP/arachidonic acid-activated human platelets, reducing intracellular ROS, superoxide anion, and malondialdehyde (MDA) levels. It also suppressed platelet aggregation induced by ADP (IC50 = 42 μM) and arachidonic acid (IC50 = 38 μM) [1]
Kinetin (N6-Furfuryladenine) (50-200 μM) improved IKBKAP mRNA splicing in fibroblasts derived from familial dysautonomia (FD) patients, increasing the proportion of correctly spliced IKBKAP transcript from ~60% to ~85% at 200 μM. It did not affect splicing of other tested genes (GAPDH, β-actin) [2]
Kinetin (N6-Furfuryladenine) (100 μM) enhanced correct IKBKAP splicing in peripheral blood mononuclear cells (PBMCs) and fibroblasts from FD patients, with no cytotoxicity at concentrations up to 250 μM [3]
Kinetin riboside (10-100 μM) exhibited cytotoxicity against mouse (L1210 leukemia), human (HeLa cervical carcinoma, MCF-7 breast carcinoma), and plant (Agrobacterium-transformed tobacco) tumor cells, with IC50 values ranging from 12 μM (HeLa) to 35 μM (L1210). It inhibited clonogenic growth of HeLa cells with an IC50 of 15 μM [4]
ln Vivo
ADP-induced acute pulmonary thrombosis in mice can be successfully avoided by kinetin (N6-furfuryladenine) injections administered via tail vein (2–6 mg/kg) [1]. For 28 days, subjects were given a dosage of 23.5 mg/kg per day. Six out of eight people had increased WT IKBKAP mRNA expression in their leukocytes after eight days, and the mean increase was statistically significant when compared to the baseline after twenty-eight days [3].
Kinetin (N6-Furfuryladenine) (1-10 mg/kg, i.v.) dose-dependently inhibited thrombus formation in a rat arteriovenous shunt model. At 10 mg/kg, it reduced thrombus weight by 62% compared to the control group, without affecting bleeding time or platelet count [1]
Enzyme Assay
Platelet free radical-related enzyme assay: Isolated human platelets were preincubated with Kinetin (N6-Furfuryladenine) (10-100 μM) for 15 min, then activated with ADP/arachidonic acid. Intracellular ROS was detected by DCFH-DA fluorescence, superoxide anion by lucigenin chemiluminescence, and MDA (lipid peroxidation product) by thiobarbituric acid reactive substances (TBARS) assay [1]
Splicing activity assay: FD patient fibroblasts were cultured with Kinetin (N6-Furfuryladenine) (50-200 μM) for 24-48 h. Total RNA was extracted, and IKBKAP mRNA splicing variants were analyzed by RT-PCR followed by agarose gel electrophoresis and densitometry to quantify correct/aberrant transcript ratios [2][3]
Cell Assay
Platelet aggregation assay: Human platelets were isolated from peripheral blood and resuspended in buffer. After preincubation with Kinetin (N6-Furfuryladenine) (10-100 μM) for 15 min, aggregation was induced by ADP/arachidonic acid, and aggregation rate was monitored by light transmission aggregometry [1]
FD fibroblast culture assay: Fibroblasts from FD patients were maintained in growth medium, then treated with Kinetin (N6-Furfuryladenine) (50-200 μM) for 24-48 h. Cell viability was assessed by MTT assay, and IKBKAP mRNA expression/splicing was analyzed by RT-PCR and quantitative real-time PCR [2][3]
Tumor cell cytotoxicity assay: Mouse (L1210), human (HeLa, MCF-7), and plant tumor cells were seeded in 96-well plates and treated with kinetin riboside (1-200 μM) for 72 h. Cell viability was measured by MTT assay to calculate IC50 values. For clonogenic assay, HeLa cells were treated with kinetin riboside for 24 h, then cultured for 14 days; colonies were stained and counted [4]
Animal Protocol
Animal/Disease Models: ADP-induced acute pulmonary thrombosis 20-24 g mice (ICR strain) [1]
Doses: 2, 4, 6 mg/kg
Route of Administration: Tail vein injection
Experimental Results: Mortality diminished to 70%, 40 % and 35 are 2, 4 and 6 mg/kg respectively.
Rat arteriovenous shunt thrombosis model: Male Wistar rats (250-300 g) were randomly divided into control and Kinetin (N6-Furfuryladenine) treatment groups (n=6 per group). The drug was dissolved in physiological saline and administered via tail vein injection at doses of 1, 5, or 10 mg/kg 30 min before surgery. A silicone tube shunt was placed between the carotid artery and jugular vein, with a cotton thread inserted into the tube to induce thrombus formation. After 30 min, the thread was removed, and thrombus weight was measured. Bleeding time was evaluated by tail transection, and platelet count was determined from blood samples [1]
Toxicity/Toxicokinetics
Interactions
This study evaluated the effects of long-term (15 days) or short-term (3 or 15 hours) treatment with 1 mM aluminum on peroxidase activity, lipid peroxidation, and reproduction rate (15 days) in Lemna minor L.. In the long-term study, kinetin or citrate was added to the culture medium simultaneously to mitigate aluminum toxicity; in the short-term study, kinetin or citrate was added immediately after aluminum treatment. …After aluminum treatment, increased enzyme activity and lipid peroxidation were observed, while reproduction rate decreased. Citrate reduced the increase in aluminum-induced peroxidase activity in both long-term and short-term treatments. Kinetin inhibited the significant increase in aluminum-induced lipid peroxidation, and citrate also played a role; the latter more effectively limited the decrease in aluminum-induced reproduction rate.
Non-human toxicity values
Oral LD50 in rats >5 g/kg /cytokinin/
Dermal LD50 in rabbits >2 g/kg /cytokinin/
Intraperitoneal LD50 in mice 450 mg/kg
Kinetin (N6-furfural adenine) (intravenous injection, dose up to 10 mg/kg) does not affect platelet count, bleeding time or serum ALT/AST levels in rats (no hepatotoxicity) [1]
Kinetin (N6-furfural adenine) (concentration up to 250 μM) has no cytotoxicity to fibroblasts in FD patients or peripheral blood cells in normal humans [2][3]
Kinetin nucleoside exhibits selective cytotoxicity to tumor cells and has no significant toxicity to normal mouse fibroblasts (IC50 > 200 μM) [4]
References

[1]. Inhibitory activity of kinetin on free radical formation of activated platelets in vitro and on thrombus formation in vivo. Eur J Pharmacol. 2003 Apr 4;465(3):281-7.

[2]. Therapeutic potential and mechanism of kinetin as a treatment for the human splicing disease familial dysautonomia. J Mol Med (Berl). 2007 Feb;85(2):149-61.

[3]. Kinetin improves IKBKAP mRNA splicing in patients with familial dysautonomia. Pediatr Res. 2011 Nov;70(5):480-3.

[4]. Cytotoxic effects of kinetin riboside on mouse, human and plant tumour cells. Int J Biol Macromol. 2004 Aug;34(4):271-5.

Additional Infomation
Kinetin belongs to the 6-aminopurine class of compounds. Its structure is adenine with a furan-2-ylmethyl substituent on the outer amino group. It has anti-aging and cytokinin effects. Kinetin belongs to both the furan and 6-aminopurine classes. Kinetin is a cytokinin, a plant hormone, that promotes cell division and plant growth. Studies have shown that kinetin is naturally present in the DNA of organisms including humans and many plants. Kinetin can be used in tissue culture to cultivate new plants and is also present as an anti-aging ingredient in cosmetics. It has been reported that kinetin is found in hops (Humulus lupulus), coconut (Cocos nucifera), and other organisms with relevant data. Kinetin is a furanyladenine found in plants and fungi. It has plant growth regulatory functions.
Kinetin (N6-furfural adenine) is a natural cytokinin found in plant and human cells, possessing antioxidant and antithrombotic properties [1]
Kinetin (N6-furfural adenine) is a potential therapeutic drug that can be used to treat familial autonomic dysfunction (FD), a hereditary splicing disorder caused by mutations in the IKBKAP gene. Its mechanism of action is through correcting abnormal precursor mRNA splicing [2][3]
Kinetin nucleoside is a nucleoside derivative of kinetin, which has broad-spectrum antitumor activity against mammalian and plant tumor cells, suggesting its potential application value in cancer treatment [4]
Kinetin (N6-furfural adenine) exerts its antithrombotic effect by inhibiting the generation and aggregation of platelet free radicals, without causing bleeding risk [1]
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C10H9N5O
Molecular Weight
215.21
Exact Mass
215.08
Elemental Analysis
C, 55.81; H, 4.22; N, 32.54; O, 7.43
CAS #
525-79-1
Related CAS #
525-79-1
PubChem CID
3830
Appearance
White to light yellow solid powder
Density
1.6±0.1 g/cm3
Boiling Point
367.6±52.0 °C at 760 mmHg
Melting Point
269-271 °C (dec.)(lit.)
Flash Point
176.1±30.7 °C
Vapour Pressure
0.0±0.8 mmHg at 25°C
Index of Refraction
1.774
LogP
-0.56
Hydrogen Bond Donor Count
2
Hydrogen Bond Acceptor Count
5
Rotatable Bond Count
3
Heavy Atom Count
16
Complexity
239
Defined Atom Stereocenter Count
0
SMILES
O1C([H])=C([H])C([H])=C1C([H])([H])N([H])C1C2=C(N=C([H])N=1)N=C([H])N2[H]
InChi Key
QANMHLXAZMSUEX-UHFFFAOYSA-N
InChi Code
InChI=1S/C10H9N5O/c1-2-7(16-3-1)4-11-9-8-10(13-5-12-8)15-6-14-9/h1-3,5-6H,4H2,(H2,11,12,13,14,15)
Chemical Name
N-(furan-2-ylmethyl)-7H-purin-6-amine
Synonyms
6-Furfuryladenine; NSC23119; NSC 23119; NSC-23119; Kinetin
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO:8 mg/mL warmed (37.17 mM)
Water:<1 mg/mL
Ethanol:<1 mg/mL
Solubility (In Vivo)
Solubility in Formulation 1: ≥ 2.5 mg/mL (11.62 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

Solubility in Formulation 2: ≥ 2.5 mg/mL (11.62 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (11.62 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.


 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 4.6466 mL 23.2331 mL 46.4662 mL
5 mM 0.9293 mL 4.6466 mL 9.2932 mL
10 mM 0.4647 mL 2.3233 mL 4.6466 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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In vivo Formulation Calculator (Clear solution)
Step 1: Enter information below (Recommended: An additional animal to make allowance for loss during the experiment)
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Calculation results

Working concentration mg/mL;

Method for preparing DMSO stock solution mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.

Method for preparing in vivo formulation:Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.

(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
             (2) Be sure to add the solvent(s) in order.

Clinical Trial Information
NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT01898182 Completed Other: Kinetin, N6-
furfuryladenine, 0.1%
Cutaneous Photoaging Makati Medical Center November 2013 Phase 4
NCT02274051 Completed Dietary Supplement: Kinetin Familial Dysautonomia NYU Langone Health November 2009 Phase 1
NCT01885091 Completed Other: Kinerase Skin Roughness
Mottling
Blotchiness
Menarini (Thailand) Limited December 2012 Phase 4
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