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Alan T Mcgown - One of the best experts on this subject based on the ideXlab platform.

  • the synthesis of indanones related to Combretastatin a 4 via microwave assisted nazarov cyclization of chalcones
    Tetrahedron Letters, 2006
    Co-Authors: Nicholas J Lawrence, Simon E M Armitage, Benjamin Greedy, Darren Cook, Sylvie Ducki, Alan T Mcgown
    Abstract:

    A fast and efficient microwave-assisted synthesis of Combretastatin A-4-like indanones has been developed. Microwave irradiation provides a useful alternative to traditional heating techniques to promote the TFA-catalyzed Nazarov cyclization of chalcones.

  • Synthesis and anticancer activity of fluorinated analogues of Combretastatin A-4
    Journal of Fluorine Chemistry, 2003
    Co-Authors: Nicholas J Lawrence, Alan T Mcgown, Lucy Annette Hepworth, David Rennison, John A Hadfield
    Abstract:

    Abstract The synthesis of a series of fluorinated benzaldehydes and their use in the Wittig synthesis of fluoro-substituted stilbenes is described. 3,5-Difluoro-4-hydroxybenzaldehyde (6) and 3-fluoro-4-methoxybenzaldehyde (11) are prepared by Duff formylation of 3,5-difluorophenol and 2-fluoroanisole, respectively. 2-Methoxy-3,4-difluorobenzaldehyde was obtained by Friedel–Crafts formylation of 2,3-difluoroanisole with α,α-dichloromethyl methyl ether. The aldehydes were used to make a series of fluorinated analogues of the anticancer Combretastatins A-1, A-2 and A-4. The in vitro anticancer properties of the fluoro Combretastatins are reported. The most active fluoro analogue 3-deoxy-3-fluoro-Combretastatin A-4 (Z-2) retains the potent cell growth inhibitory properties of CA-4.

  • Novel syntheses of cis and trans isomers of Combretastatin A-4.
    The Journal of organic chemistry, 2001
    Co-Authors: Keira Gaukroger, Nicholas J Lawrence, John A Hadfield, Lucy Annette Hepworth, Alan T Mcgown
    Abstract:

    A high-yielding, two-step stereoselective synthesis of the anticancer drug (Z)-Combretastatin A-4 (1) has been devised. The method uses the Perkin condensation of 3,4,5-trimethoxyphenylacetic acid and 3-hydroxy-4-methoxybenzaldehyde followed by decarboxylation of the cinnamic acid intermediate using copper and quinoline. The iodine-catalyzed isomerization of the Z isomer 1 results in complete conversion to the E isomer. The Suzuki cross-coupling of an aryl boronic acid and vinyl bromide has also been successfully employed to produce both Z and E isomers of Combretastatin A-4 stereoselectively. Both methods are far superior to the current five-step Wittig synthesis in which both isomers are produced nonstereoselectively.

  • Antimitotic and cell growth inhibitory properties of Combretastatin A-4-like ethers.
    Bioorganic & medicinal chemistry letters, 2001
    Co-Authors: Nicholas J Lawrence, Alan T Mcgown, David Rennison, Meiki Woo, John A Hadfield
    Abstract:

    Abstract A series of diarylamines, diaryl and arylbenzyl ethers based on Combretastatin A-4 was prepared and evaluated for anticancer activity. 2-Methoxy-5-(3′,4′,5′-trimethoxyphenoxymethyl)phenol was the most active (IC 50 , K562 20 nM) and caused significant G2/M cell cycle arrest.

  • In vivo and in vitro evaluation of Combretastatin A-4 and its sodium phosphate prodrug.
    British journal of cancer, 1999
    Co-Authors: K Grosios, Alan T Mcgown, George R Pettit, S E Holwell, M C Bibby
    Abstract:

    The anti-tumour effects and mechanism of action of Combretastatin A-4 and its prodrug, Combretastatin A-4 disodium phosphate, were examined in subcutaneous and orthotopically transplanted experimental colon tumour models. Additionally, the ability of these compounds to directly interfere with endothelial cell behaviour was also examined in HUVEC cultures. Combretastatin A-4 (150 mg kg–1, intraperitoneally (i.p.)) and its water-soluble prodrug (100 mg kg–1, i.p.) caused almost complete vascular shutdown (at 4 h), extensive haemorrhagic necrosis which started at 1 h after treatment and significant tumour growth delay in MAC 15A subcutaneous (s.c.) colon tumours. Similar vascular effects were obtained in MAC 15 orthotopic tumours and SW620 human colon tumour xenografts treated with the prodrug. More importantly, in the orthotopic models, necrosis was seen in vascularized metastatic deposits but not in avascular secondary deposits. The possible mechanism giving rise to these effects was examined in HUVEC cells. Here cellular networks formed in type I calf-skin collagen layers and these networks were completely disrupted when incubated with a non-cytotoxic concentration of Combretastatin A-4 or its prodrug. This effect started at 4 h and was complete by 24 h. The same non-cytotoxic concentrations resulted in disorganization of F-actin and β-tubulin at 1 h after treatment. In conclusion, Combretastatin A-4 and its prodrug caused extensive necrosis in MAC 15A s.c. and orthotopic colon cancer and metastases, resulting in anti-tumour effects. Necrosis was not seen in avascular tumour nodules, suggesting a vascular mechanism of action. © 1999 Cancer Research Campaign

Mouad Alami - One of the best experts on this subject based on the ideXlab platform.

George R Pettit - One of the best experts on this subject based on the ideXlab platform.

  • an efficient synthetic strategy for obtaining 4 methoxy carbon isotope labeled Combretastatin a 4 phosphate and other z Combretastatins
    Journal of Natural Products, 2010
    Co-Authors: George R Pettit, Fiona Hogan, Mathew D Minardi, P B Price
    Abstract:

    Human cancer and other clinical trials under development employing Combretastatin A-4 phosphate (1b, CA4P) should benefit from the availability of a [11C]-labeled derivative for positron emission tomography (PET). In order to obtain a suitable precursor for addition of a [11C]methyl group at the penultimate step, several new synthetic pathways to CA4P were evaluated. Geometrical isomerization (Z to E) proved to be a challenge, but it was overcome by development of a new CA4P synthesis suitable for 4-methoxy isotope labeling.

  • Evaluation of Combretastatin A-4 prodrug in a non-Hodgkin's lymphoma xenograft model: preclinical efficacy.
    Anti-cancer drugs, 2001
    Co-Authors: Sanaa Nabha, George R Pettit, Ramzi M. Mohammad, Nathan R. Wall, Julie A. Dutcher, Bashar M Salkini, Ayad Al-katib
    Abstract:

    Combretastatin A-4 prodrug (CA4P) is a new antitubulin agent currently in phase I/II clinical trials against solid tumors. We have previously reported on the in vitro activity of CA4P against a panel of malignant human B-lymphoid cell lines. In this study, we investigated the antitumor and the antia

  • Effects of Combretastatin A-4 prodrug against a panel of malignant human B-lymphoid cell lines
    Anti-cancer drugs, 2000
    Co-Authors: Sanaa Nabha, George R Pettit, Ramzi M. Mohammad, Nathan R. Wall, Ayad Al-katib
    Abstract:

    Combretastatin A-4 (CA-4) is one of a family of compoundsisolated from the South African willow tree Combretumcaffrum. CA-4 was found to be active against murinemelanoma and a variety of other human solid tumors. Forthe first time, we report the effect of CA-4 against a panel ofmalignant human B-lymphoid cell lines [early pre-B acutelymphoblastic leukemia (Reh), diffuse large cell lymphoma(WSU-DLCL

  • In vivo and in vitro evaluation of Combretastatin A-4 and its sodium phosphate prodrug.
    British journal of cancer, 1999
    Co-Authors: K Grosios, Alan T Mcgown, George R Pettit, S E Holwell, M C Bibby
    Abstract:

    The anti-tumour effects and mechanism of action of Combretastatin A-4 and its prodrug, Combretastatin A-4 disodium phosphate, were examined in subcutaneous and orthotopically transplanted experimental colon tumour models. Additionally, the ability of these compounds to directly interfere with endothelial cell behaviour was also examined in HUVEC cultures. Combretastatin A-4 (150 mg kg–1, intraperitoneally (i.p.)) and its water-soluble prodrug (100 mg kg–1, i.p.) caused almost complete vascular shutdown (at 4 h), extensive haemorrhagic necrosis which started at 1 h after treatment and significant tumour growth delay in MAC 15A subcutaneous (s.c.) colon tumours. Similar vascular effects were obtained in MAC 15 orthotopic tumours and SW620 human colon tumour xenografts treated with the prodrug. More importantly, in the orthotopic models, necrosis was seen in vascularized metastatic deposits but not in avascular secondary deposits. The possible mechanism giving rise to these effects was examined in HUVEC cells. Here cellular networks formed in type I calf-skin collagen layers and these networks were completely disrupted when incubated with a non-cytotoxic concentration of Combretastatin A-4 or its prodrug. This effect started at 4 h and was complete by 24 h. The same non-cytotoxic concentrations resulted in disorganization of F-actin and β-tubulin at 1 h after treatment. In conclusion, Combretastatin A-4 and its prodrug caused extensive necrosis in MAC 15A s.c. and orthotopic colon cancer and metastases, resulting in anti-tumour effects. Necrosis was not seen in avascular tumour nodules, suggesting a vascular mechanism of action. © 1999 Cancer Research Campaign

  • Antineoplastic agents. 410. Asymmetric hydroxylation of trans-Combretastatin A-4.
    Journal of medicinal chemistry, 1999
    Co-Authors: George R Pettit, Ernest Hamel, Delbert L. Herald, Michael R. Boyd, Robin K. Pettit, Brian E. Toki, Jean Chapuis
    Abstract:

    The South African willow tree Combretum caffrum has yielded a number of potent cancer cell growth inhibitors. The present SAR studies of the antineoplastic agent Combretastatin A-4 (1c) were focused mainly on the olefinic bridge to determine the effects on cancer cell growth and, potentially, to better define the Combretastatin A-4 binding site on tubulin. The geometric trans-isomer 3a of Combretastatin A-4 was converted to the (1S,2S)- and (1R,2R)-vicinal diols 4c and 4d, respectively, under Sharpless' asymmetric dihydroxylation conditions. Cancer cell line testing showed the (1S,2S)-diol 4c to be more potent than its enantiomer 4d. Diol 4c weakly inhibited tubulin polymerization (IC50 = 22 μM, versus 1.2 μM for Combretastatin A-4), while 4d was inactive (IC50 > 40 μM). Esterification of either stereoisomer at the diol and/or phenolic positions resulted in elimination of inhibitory activity.

Olivier Provot - One of the best experts on this subject based on the ideXlab platform.

Abdallah Hamze - One of the best experts on this subject based on the ideXlab platform.