Hydrophobic segments of heat-inactivated proteins, competing with small chaperones IbpA and IbpB in E. coli [1].
Nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway [2].

In E. coli JW3663 ibpB::kan (pLeo1) cells lacking the small chaperone IbpB, 2-Undecanone (20 μmol) almost completely inhibits the DnaKJE-ClpB bichaperone-dependent refolding of heat-inactivated P. leiognathi luciferase. In E. coli BW25113 ibpAB+ (pLeo1) cells, the same treatment decreases the refolding level, but not completely [1].
In E. coli JW3663 ibpB::kan (pLeo3) cells, 2-Undecanone (20 μmol) almost completely inhibits the refolding of heat-inactivated P. leiognathi luciferase, whereas in E. coli BW25113 ibpAB+ (pLeo3) cells, the refolding level is decreased to 40% [1].
In BEAS-2B cells, 2-Undecanone (25, 50, or 100 μM) for 48 hours significantly protects cells from B[a]P-induced cytotoxicity, increasing cell viability in a dose-dependent manner compared to B[a]P treatment alone [2].
2-Undecanone (25, 50, or 100 μM) for 48 hours markedly increases the proliferation rate of BEAS-2B cells treated with B[a]P (5 μM), as measured by EdU incorporation [2].
2-Undecanone (25, 50, or 100 μM) for 48 hours significantly decreases the percentage of BEAS-2B cells arrested in the G0/G1 phase by B[a]P (5 μM) and significantly reverses the B[a]P-induced suppression of cyclin D1 protein levels [2].
2-Undecanone (25, 50, or 100 μM) for 48 hours attenuates B[a]P-induced DNA damage in BEAS-2B cells, as demonstrated by decreased fluorescence and reduced migrated tails of damaged DNA in a comet assay [2].
2-Undecanone (25, 50, or 100 μM) for 48 hours significantly decreases B[a]P-induced high expression of the DNA damage marker p-H2A.X in a dose-dependent manner in BEAS-2B cells [2].
2-Undecanone (25, 50, or 100 μM) for 24 hours significantly attenuates B[a]P-induced increases in IL-1β protein levels in cell culture supernatants and also diminishes increases in pro-IL-1β and IL-1β protein levels in cell lysates of BEAS-2B cells [2].
2-Undecanone (25, 50, or 100 μM) for 48 hours significantly reduces B[a]P-mediated intracellular ROS overproduction in a dose-dependent manner in BEAS-2B cells [2].
2-Undecanone (50 μM) significantly increases the protein levels of Nrf2, HO-1, and NQO-1 in whole-cell lysates and results in significant increases in nuclear Nrf2 protein levels in BEAS-2B cells. It also notably promotes the translocation of Nrf2 from the cytoplasm to the nucleus [2].
2-Undecanone markedly attenuates the downregulation of Nrf2, HO-1, and NQO-1 expression induced by B[a]P (5 μM) in BEAS-2B cells [2].
Transfection of BEAS-2B cells with Nrf2-specific siRNA (siNrf2-1 or siNrf2-2) significantly attenuates the 2-Undecanone-induced increases in HO-1 and NQO-1 protein levels [2].
The reduction in B[a]P-induced ROS overproduction, DNA damage (p-H2A.X), and inflammation (IL-1β) caused by 2-Undecanone is markedly diminished by transfection with siNrf2-1 or siNrf2-2 in BEAS-2B cells [2].
The protective effects of 2-Undecanone (50 μM) against B[a]P-induced cytotoxicity are markedly attenuated by siNrf2 transfection in BEAS-2B cells [2].

In an A/J mouse model of B[a]P-induced lung tumorigenesis, 2-Undecanone (100 or 200 mg/kg) administered five times a week for 38 weeks significantly decreased the mean number of lung tumors. The corresponding tumor inhibition rates were 33.62 ± 14.60% (p < 0.05) and 38.26 ± 13.59% (p < 0.01), respectively, compared to control mice given B[a]P [2].
2-Undecanone (100 or 200 mg/kg) treatment significantly downregulated p-H2A.X expression in the lung tissues of B[a]P-treated mice [2].
2-Undecanone (100 or 200 mg/kg) treatment significantly downregulated IL-1β levels in the plasma of B[a]P-treated mice [2].
Immunohistochemistry of mouse lung tissues showed that 2-Undecanone (100 or 200 mg/kg) treatment strikingly enhanced the expression of Nrf2, HO-1, and NQO-1 in a dose-dependent manner compared to B[a]P treatment alone [2].

Cell Viability (MTT Assay): BEAS-2B cells were seeded in 96-well plates for 24 hours before treatment. Cells were exposed to 2-Undecanone (0-200 μM) alone or B[a]P (5 μM) plus 2-Undecanone (0-200 μM) for 48 hours. After incubation, MTT solution was added to each well and incubated at 37°C for 4 hours. The medium was then removed, and the intracellular formazan was solubilized with DMSO. Absorbance was read at 570 nm to calculate cell viability as a percentage of the control [2].
Cell Proliferation (EdU Assay): BEAS-2B cells were seeded into 96-well plates and exposed to B[a]P (5 μM) alone or B[a]P (5 μM) plus 2-Undecanone (25, 50, or 100 μM) for 48 hours. After incubation, cells were incubated with EdU labeling medium for 24 hours, fixed with paraformaldehyde, and incubated with glycine. Cells were then incubated with Apollo 488 working solution, washed, and stained with Hoechst 33342 dye. Images were captured, and the percentage of EdU-positive cells was calculated from random fields [2].
Cell Cycle Assay: BEAS-2B cells were seeded in 6-well plates and exposed to B[a]P (5 μM) alone or B[a]P (5 μM) plus 2-Undecanone (25, 50, or 100 μM) for 48 hours. Cells were then harvested, fixed with cold ethanol at 4°C overnight, and stained with propidium iodide. The cell cycle was detected by flow cytometry and analyzed with software [2].
Western Blot Analysis: Treated BEAS-2B cells were lysed using RIPA buffer containing a protease inhibitor cocktail. Nuclear protein extracts were also prepared. Protein concentrations were determined with a BCA kit. Western blotting was performed to detect protein levels of cyclin D1, p-H2A.X, IL-1β, pro-IL-1β, Nrf2, HO-1, and NQO-1 [2].
Comet Assay: BEAS-2B cells were seeded in 6-well plates and exposed to B[a]P (5 μM) alone or B[a]P (5 μM) plus 2-Undecanone (25, 50, or 100 μM) for 48 hours. Cells were harvested and suspended in low-melting point agarose, then spread on agarose-coated slides. Slides were immersed in cell lysis solution at 4°C, then transferred to an electrophoretic box. Electrophoresis was performed at 4°C. Slides were then washed, stained with EB solution, and images were captured using a fluorescence microscope [2].
Immunofluorescence: BEAS-2B cells on confocal dishes were exposed to B[a]P (5 μM) alone or B[a]P (5 μM) plus 2-Undecanone (25, 50, or 100 μM) for 48 hours. Cells were fixed in cold methanol, permeabilized with TritonX-100, and blocked with bovine serum albumin. Cells were then incubated with a p-H2A.X or Nrf2 antibody, then stained with a secondary fluorescent antibody and DAPI. Fluorescence signals were detected using a confocal fluorescence microscope [2].
Intracellular ROS Measurement: BEAS-2B cells in six-well plates were exposed to B[a]P (5 μM) alone or B[a]P (5 μM) plus 2-Undecanone (25, 50, or 100 μM) for 48 hours. Cells were washed and incubated with a ROS detection reagent (CM-H2DCFDA) for 30 minutes at 37°C. Fluorescence signals were detected by flow cytometry or a fluorescence microscope [2].
siRNA Interference: BEAS-2B cells were transfected with 50 nM Nrf2-targeting siRNA (siNrf2) or control siRNA (siCon) using a transfection kit. After 24 hours of transfection, cells were exposed to treatments. At the end of treatment, cells were collected for Western blot analysis, ROS measurement, or MTT assay [2].

B[a]P-Induced Lung Cancer Model: Male A/J mice (4-6 weeks old, 18-22 g) were intraperitoneally injected with B[a]P (100 mg/kg) at the 1st week. Two weeks later, from the 3rd to the 38th week, mice were orally administered 2-Undecanone (100 or 200 mg/kg) five times a week. A control group received B[a]P in a sterilized corn oil vehicle. At the end of the treatment (38 weeks), mice were sacrificed. Lung images were captured, and lungs were collected for analysis [2].

Non-Human Toxicity Values
Rat oral LD50 >5 g/kg; Mouse oral LD50 3.88 g/kg; Rabbit (male and female) dermal LD50 >2 g/kg /Data from table/

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No considerable differences were observed in the organ indexes (heart, kidney, thymus, liver, and spleen) between the B[a]P control group and the 2-Undecanone treatment groups in A/J mice. There were no significant body weight differences between the control group and the treatment group during the experiment [2].
Incubation with 2-Undecanone (up to 200 μM) alone for 48 hours did not change or weakly decreased BEAS-2B cell viability, indicating low cytotoxicity [2].

[1]. Ketones 2-heptanone, 2-nonanone, and 2-undecanone inhibit DnaK-dependent refolding of heat-inactivated bacterial luciferases in Escherichia coli cells lacking small chaperon IbpB. Appl Microbiol Biotechnol. 2017 Jul;101(14):5765-5771.

[2]. Houttuynia cordata Thunb. and its bioactive compound 2-undecanone significantly suppress benzo(a)pyrene-induced lung tumorigenesis by activating the Nrf2-HO-1/NQO-1 signaling pathway. J Exp Clin Cancer Res. 2019 Jun 7;38(1):242.

Undecane-2-one is a dialkyl ketone with a methyl and a nonyl alkyl group. It is used as a rodenticide and as a plant metabolite. It is both a dialkyl ketone and a methyl ketone. 2-Undecane-one has been reported in Francisella tularensis, Zanthoxylum myriacanthum, and other organisms with relevant data. 2-Undecane-one is a metabolite found or produced by Saccharomyces cerevisiae.

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2-Undecanone is a volatile ketone produced by Pseudomonas chlororaphis strain 449 [1].
2-Undecanone is used as a standard marker for quality control of Houttuynia cordata Thunb. in the Chinese Pharmacopoeia [2].
The inhibitory activity of ketones on DnaK-dependent refolding of heat-inactivated luciferases increases in the series: 2-pentanone, 2-undecanone, 2-heptanone, and 2-nonanone. 2-Undecanone (20 μmol required for inhibition) is less active than 2-nonanone (2.5 μmol) and 2-heptanone (10 μmol) but more active than 2-pentanone (60 μmol, only incomplete inhibition) [1].
2-Undecanone can effectively activate the Nrf2-HO-1/NQO-1 signaling pathway to counteract intracellular ROS generation, thereby attenuating DNA damage and inflammation induced by B[a]P stimulation and playing a role in the chemoprevention of B[a]P-induced lung tumorigenesis [2].

C11H22O

170.2918

170.167

112-12-9

8163

Colorless to light yellow liquid

0.8±0.1 g/cm3

230.8±3.0 °C at 760 mmHg

11-13 °C(lit.)

88.9±0.0 °C

0.1±0.4 mmHg at 25°C

1.425

4.09

0

1

8

12

108

0

O=C(C([H])([H])[H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])[H]

KYWIYKKSMDLRDC-UHFFFAOYSA-N

InChI=1S/C11H22O/c1-3-4-5-6-7-8-9-10-11(2)12/h3-10H2,1-2H3

undecan-2-one

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~100 mg/mL (~587.20 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (14.68 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.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (14.68 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 (14.68 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.

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 (Please use freshly prepared in vivo formulations for optimal results.)