Honokiol

Catalog No.S2310

Honokiol Chemical Structure

Molecular Weight(MW): 266.334

Honokiol is the active principle of magnolia extract that inhibits Akt-phosphorylation and promotes ERK1/2 phosphorylation. Phase 3.

Size Price Stock Quantity  
In DMSO USD 110 In stock
USD 88 In stock
USD 148 In stock
USD 260 In stock
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Cited by 7 Publications

2 Customer Reviews

  • (B) Cleaved PARP, Bax and Bcl2 protein expression was evaluated by immunoblotting of KRAS mutant cells lysates after 48 h of honokiol (10, 20, 40, and 60 μM) treatment. ∗∗P < 0.01 and ∗∗∗P < 0.001 for comparison between control group and honokiol-treated group.

    Front Pharmacol, 2017, 8:199. Honokiol purchased from Selleck.

    Lyn, p-Lyn, EGFR, p-EGFR, PI3K, p-PI3K, AKT, p-AKT, STAT3, and p-STAT3 protein expression of PC-9 cells were detected by Western blots assay after treated with honokiol (0, 20, 40, and 60 μM) for 24 h. The non-specific Src tyrosine kinase inhibitor (TKI) PP2 is the positive control.

    Front Pharmacol, 2018, 9:558. Honokiol purchased from Selleck.

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Choose Selective Akt Inhibitors

Biological Activity

Description Honokiol is the active principle of magnolia extract that inhibits Akt-phosphorylation and promotes ERK1/2 phosphorylation. Phase 3.
Targets
Akt-phosphorylation [1] MEK [1]
In vitro

Honokiol shows pro-apoptotic effects in melanoma, sarcoma, myeloma, leukemia, bladder, lung, prostate, oral squamous cell carcinoma and colon cancer cell lines. Honokiol is effective on inducing apoptosis in SVR angiosarcoma cells. Treatment of SVR cells with honokiol causes decreased phosphorylation of MAP kinase, akt, and c-src. In addition, honokiol potentiates TRAIL-mediated apoptosis, and honokiol cytotoxicity is partially abrogated by neutralizing antibodies to TRAIL. Honokiol also has direct antiangiogenic activity, in that honokiol blocks the phosphorylation and rac activation due to VEGF-VEGFR2 interactions. [1] Honokiol causes apoptosis in CLL cells through activation of caspase 8, followed by caspase 9 and 3 activation. Honokiol prevents interleukin-4-mediated survival of CLL cells, and potentiats the cytotoxicity of chlorambucil, fludarabine, and cladribine. [3] Honokiol kills myeloma cells from relapsed patients at doses that does not kill PBMCs. Caspase 3, 7, 8, and 9 are induced by honokiol treatment, as well as PARP cleavage. [2] Honokiol is found to induce apoptosis in the colon cancer cell lines RKO. [4] Honokiol potentiates apoptosis, suppresses osteoclastogenesis, and inhibits invasion through modulation of nuclear factor-kappaB activation pathway. [5] Honokiol may act as a potent anti-inflammatory agent with multipotential activities due to an inhibitory effect on the PI3K/Akt pathway. [6]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human UACC-903 cells M2nYbmN6fG:2b4jpZ4l1gSCjc4PhfS=> M{\5T2N6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJHVCS0NvOUCzJINmdGy|IHHmeIVzKDd{IHjyd{BjgSCPVGOgZZN{[XluIFnDOVA:PS5zIN88US=> NEXVZ3gzOjV|M{m4Ny=>
Vero E6 cells NYnSPVVPTnWwY4Tpc44h[XO|YYm= MYHBcpRqfmm{YXygZYN1cX[rdImgZYdicW6|dDDTRXJUKGOxcn;uZZZqenW|IHnuJHZmem9iRU[gZ4VtdHNiYYPz[ZN{\WRiYYOgbY5pcWKrdHnvckBw\iC4aYLhcEBz\XCuaXPheIlwdiCkeTDFUGlUSSxiRVO1NF03NjVizszN M13jRlE4PjZ|NUO5
human UACC-903 cells NH;K[YdEgXSxdH;4bYNqfHliYYPzZZk> MX;DfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDVRWNENTlyMzDj[YxteyCjZoTldkAzPCCqcoOgZpkhVVSVIHHzd4F6NCCLQ{WwQVcvPDVizszN MmnWNlI2OzN7OEO=
human A549 cells NFqyZ5REgXSxdH;4bYNqfHliYYPzZZk> M{PvOGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGE2PDliY3XscJMh[W[2ZYKgO|IhcHK|IHL5JG1VWyCjc4PhfUwhUUN3ME23Mlc2KM7:TR?= NGn5U5ozOjV|M{m4Ny=>
human CEM cells MlLmR5l1d3SxeHnjbZR6KGG|c3H5 NGHQPGREgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBETU1iY3XscJMtKEmFNUC9NVAvQSEQvF2= M1vZO|E4PTh5NUey
HEK293 cells NGr3V5VHfW6ldHnvckBie3OjeR?= M3LpU2Fod26rc4SgZYN1cX[rdImgZZQhWliUYXzwbIEhcW5iSFXLNlk{KGOnbHzzJIF{e2W|c3XkJIF{KHS{YX7zZ5JqeHSrb37hcEBi[3SrdnH0bY9vKGGodHXyJFQ5KGi{czDifUBtfWOrZnXyZZNmKHKncH;yeIVzKGenbnWgZZN{[XluIFXDOVA:OTFwODFOwG0> MYGyNFY6PTR5Mh?=
human A549 cell NELrXHlEgXSxdH;4bYNqfHliYYPzZZk> MUWyOEBp MnyzR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gRVU1QSClZXzsd{Bi\nSncjCyOEBpenNiYomgUXRUKGG|c3H5MEBKSzVyPUGyMlUyKM7:TR?= NFXCbXkzOjV|M{m4Ny=>
human HT-29 cells NU[0TXJ7S3m2b4TvfIlkcXS7IHHzd4F6 MljxO|IhcA>? NYDaOmVkS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hUFRvMkmgZ4VtdHNiYX\0[ZIhPzJiaILzJIJ6KE2WUzDhd5NigSxiSVO1NF0yOy5{NDFOwG0> MWSyNlU{Ozl6Mx?=
human PBM cells MkCzR5l1d3SxeHnjbZR6KGG|c3H5 MYHDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDQRm0h[2WubIOsJGlEPTB;MU[uNUDPxE1? NELWZnEyPzV6N{W3Ni=>
Hep-G2 cells M3frV2N6fG:2b4jpZ4l1gSCjc4PhfS=> M{jVXWN6fG:2b4jpZ4l1gSCxZjDjc41xd3WwZDDh[4FqdnO2IHj1cYFvKGyrdnXyJJR2dW:{IHPlcIwhdGmwZTCoTIVxNUd{KTD3ZZMh\GW2ZYLtbY5m\CxiSVO1NF0yPi53IN88US=> MXmxOVU5OjR|Mh?=
human HepG2 cells NVHCSYg4WHKxbHnm[ZJifGmxbjDhd5NigQ>? NEfJcYwzPCCq MUHBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKEincFeyJINmdGy|IHHmeIVzKDJ2IHjyd{BjgSCPVGSgZZN{[XluIFnDOVA:OTZwNTFOwG0> NUDjVYFlOjF6NUO5PVE>
human K562 cells MnrlVJJwdGmoZYLheIlwdiCjc4PhfS=> NFXydmRCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFu1OlIh[2WubIOgZpkhVVSWIHHzd4F6NCCLQ{WwQVIyNjFizszN MkLsNVk2QDl4N{i=
Vero cells MYXDfZRwfG:6aXPpeJkh[XO|YYm= MnHXR5l1d3SxeHnjbZR6KGGpYXnud5QhXmW{bzDj[YxteyxiSVO1NF0zOi53IN88US=> MXexOlczOjZ4NB?=
human A2780 cells Ml;6VJJwdGmoZYLheIlwdiCjc4PhfS=> MYnBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHPpd5Bt[XSrbj3z[Y5{cXSrdnWgbJVu[W5iQUK3PFAh[2WubIOgZpkhVVSWIHHzd4F6NCCLQ{WwQVMxNjVizszN MYqxPVU5QTZ5OB?=
human SPC-A1 cells MmDNVJJwdGmoZYLheIlwdiCjc4PhfS=> NYnmV|ZHSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDTVGMuSTFiY3XscJMh[nliTWTUJIF{e2G7LDDJR|UxRTN4LkGg{txO MonGNVk2QDl4N{i=
HUVEC cells M3LLfmZ2dmO2aX;uJIF{e2G7 NIm2WpMzOCEQvF2= NIq4ZmYzPCCq NW\pcIFFSW62aX3p[5JifG:{eTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKEiXVlXDJINmdGy|IHH0JFIxKHWPIHHmeIVzKDJ2IHjyd{BjgSC5b4Xu[E1p\WGuaX7nJIF{e2G7 NIjyUW4zOTh3M{m5NS=>
HEK293 cells MYDGeY5kfGmxbjDhd5NigQ>? MmXKNlQuPDhiaB?= MYDB[49vcXO2IHHjeIl3cXS7IHH0JIh2dWGwIGLYVk1idHCqYTDlfJBz\XO|ZXSgbY4hUEWNMkmzJINmdGy|IHPv[ZhxemW|c3nu[{B4cXSqIIDDUXgu[mW2YT3nZYwh[W[2ZYKgNlQhfG9iNEigbJJ{KGK7IHz1Z4ln\XKjc3WgdoVxd3K2ZYKg[4Vv\SCjc4PhfS=> M2rablI1QTV7OUi3
human SH-SY5Y cells NXvvcoRkTnWwY4Tpc44h[XO|YYm= MVixNEDPxE1? NH;vdYg{OCCvaX7z MlnFUoV2em:ycn;0[YN1cX[nIHHjeIl3cXS7IHnuJIh2dWGwIGPIMXN[PVliY3XscJMh[XO|ZYPz[YQh[XNiaX7obYJqfGmxbjDv[kBEUFBiYX7kJHRDUFBvaX7keYNm\CClZXzsJIRm[XSqIHH0JFExKHWPIHnuZ5Vj[XSnZDDmc5IhOzBibXnud{BxemmxcjD0c{BkcGGubHXu[4UhdWWjc4Xy[YQh[W[2ZYKgN{BpenNiYomgUXRVKGG|c3H5 Ml36NlIyPDJ3M{m=

... Click to View More Cell Line Experimental Data

Assay
Methods Test Index PMID
Western blot
p-EGFR / p-AKT / p-STAT3 / p-ERK / p-GSK3α/β / Bax / p-pRb / p-BAD / IκBα / CDK2 / CDK4 / Cyclin D1; 

PubMed: 27458163     


Honokiol differentially modulated the level of EGFR and its downstream effectors in 1170 cells in a dose-dependent manner. Cells were treated with the different concentrations of honokiol for 72 h, and cell lysates were analyzed by Western immunoblotting as described in Material and Methods. At least three independent assays were carried out using cell lysates prepared on different days.

p-Lyn / Lyn / p-PI3K ; 

PubMed: 29892225     


Lyn, p-Lyn, EGFR, p-EGFR, PI3K, p-PI3K, AKT, p-AKT, STAT3, and p-STAT3 protein expression of PC-9 cells were detected by Western blots assay after treated with honokiol (0, 20, 40, and 60 μM) for 24 h. The non-specific Src tyrosine kinase inhibitor (TKI) PP2 is the positive control. ∗P > 0.05 and ∗∗∗P < 0.01 for comparison among groups.

27458163 29892225
Immunofluorescence
Vimentin / Occludin ; 

PubMed: 24508063     


MCF7 and MDA‐MB‐231 cells were treated with vehicle (C) or 5 μM honokiol (HNK) and subjected to immunofluorescence analysis of vimentin and occludin.

IκBα / NF-κB p65 ; 

PubMed: 27212040     


Confocal microscopy of localization and expression of IκBα (Red) and p65 (green) in ECs preincubated with DMSO or honokiol (3 μM) for 30 min, then with TNF-α (10 ng/ml) for 15 min. Bars, 10 μm. Representative images from 3 or 4 experiments are shown.

24508063 27212040
Growth inhibition assay
Cell viability; 

PubMed: 30587839     


Effect of honokiol on glioma/glioblastoma cell viability. U251 human glioma and U-87 MG human glioblastoma cells were treated with different concentrations of honokiol for 24 (A) and 48 h (B). MTT assay was used to assess cell viability. Data are presented as means ± SEM from 3 independent experiments. IC50 values for U251 and U-87 MG at 24 h were 54 μM and 62.5 μM, respectively. * p < 0.05 and ** p < 0.01 vs. vehicle control (one-way ANOVA with Tukey's post-hoc test).

30587839
In vivo Honokiol is highly effective against SVR angiosarcoma in nude mice. [1] Honokiol inhibits the growth of RKO cells in murine xenografts. [4] Honokiol prevents the growth of MDA-MD-231 breast cancer cells in murine xenografts. [7]

Protocol

Solubility (25°C)

In vitro DMSO 53 mg/mL (198.99 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+40% PEG 300+2% Tween 80+ddH2O
For best results, use promptly after mixing.
2mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 266.334
Formula

C18H18O2

CAS No. 35354-74-6
Storage powder
in solvent
Synonyms N/A

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID