cytochalasin E

{{chembox

| Verifiedfields = changed

| Watchedfields = changed

| verifiedrevid = 363722351

| Reference = [http://www.sigmaaldrich.com/catalog/ProductDetail.do?N4=C2149|SIGMA&N5=SEARCH_CONCAT_PNO|BRAND_KEY&F=SPEC Cytochalasin E from Aspergillus clavatus] at Sigma-Aldrich

| ImageFile=Cytochalasin E.png

| PIN=(4E,6R,8S,10E,11aS,11bS,12aR,13S,13aS,14S)-14-Benzyl-6-hydroxy-6,8,12a,13-tetramethyl-9,11a,11b,12a,13,13a,14,15-octahydro-2H-[1,3]dioxacyclotridecino[4,5-d]oxireno[2,3-f]isoindole-2,7,16(6H,8H)-trione

| OtherNames=

|Section1={{Chembox Identifiers

| CASNo_Ref = {{cascite|correct|??}}

| CASNo=36011-19-5

| PubChem=5458385

| ChemSpiderID_Ref = {{chemspidercite|changed|chemspider}}

| ChemSpiderID = 4572350

| ChEBI = 68201

| ChEMBL = 494856

| 3DMet = L06226

| KEGG = C19953

| InChI = 1/C28H33NO7/c1-16-9-8-12-19-23-27(4,35-23)17(2)21-20(15-18-10-6-5-7-11-18)29-24(31)28(19,21)36-25(32)34-14-13-26(3,33)22(16)30/h5-8,10-14,16-17,19-21,23,33H,9,15H2,1-4H3,(H,29,31)/b12-8+,14-13+/t16-,17-,19-,20-,21-,23-,26+,27+,28+/m0/s1

| InChIKey = LAJXCUNOQSHRJO-ZYGJITOWBM

| StdInChI_Ref = {{stdinchicite|changed|chemspider}}

| StdInChI = 1S/C28H33NO7/c1-16-9-8-12-19-23-27(4,35-23)17(2)21-20(15-18-10-6-5-7-11-18)29-24(31)28(19,21)36-25(32)34-14-13-26(3,33)22(16)30/h5-8,10-14,16-17,19-21,23,33H,9,15H2,1-4H3,(H,29,31)/b12-8+,14-13+/t16-,17-,19-,20-,21-,23-,26+,27+,28+/m0/s1

| StdInChIKey_Ref = {{stdinchicite|changed|chemspider}}

| StdInChIKey = LAJXCUNOQSHRJO-ZYGJITOWSA-N

| EINECS = 252-835-7

| SMILES=C[C@H]1C/C=C/[C@H]2[C@H]3[C@](O3)([C@H]([C@@H]4[C@]2(C(=O)N[C@H]4CC5=CC=CC=C5)OC(=O)O/C=C/[C@@](C1=O)(C)O)C)C

}}

|Section2={{Chembox Properties

| C=28 | H=33 | N=1 | O=7

| Appearance=

| Density=1.309 g/ml

| MeltingPt=

| BoilingPt=

| Solubility=

}}

|Section3={{Chembox Hazards

| MainHazards=Toxic

| GHSPictograms = {{GHS06}}{{GHS08}}

| GHSSignalWord = Danger

| HPhrases = {{H-phrases|300|310|330|361}}

| PPhrases = {{P-phrases|201|202|260|262|264|270|271|280|281|284|301+310|302+350|304+340|308+313|310|320|321|322|330|361|363|403+233|405|501}}

| FlashPt=

| AutoignitionPt =

}}

}}

Cytochalasin E, a member of the cytochalasin group, is an inhibitor of actin polymerization in blood platelets. It inhibits angiogenesis and tumor growth. Unlike cytochalasin A and cytochalasin B, it does not inhibit glucose transport. Cytochalasin E, however, was noted to decrease glucose absorption in mice around the intestinal tissues by increasing the Km needed for glucose to reach the Vmax, which meant that a higher concentration of glucose was required in its presence to attain Vmax. Since Vmax remained the same according to another study, it is evident that CE is indeed a competitive inhibitor at the intestinal receptor sites for glucose.{{Cite journal |last1=Glinsukon |first1=T. |last2=Kongsuktrakoon |first2=B. |last3=Toskulkao |first3=C. |last4=Sophasan |first4=S. |date=1983-03-01 |title=Cytochalasin E: inhibition of intestinal glucose absorption in the mouse |url=https://pubmed.ncbi.nlm.nih.gov/6836602/ |journal=Toxicology Letters |volume=15 |issue=4 |pages=341–348 |doi=10.1016/0378-4274(83)90154-6 |issn=0378-4274 |pmid=6836602}}

Because of its antiangiogenic effect, cytochalasin E is a potential drug for age-related macular degeneration, a kind of blindness caused by an abnormal proliferation of blood vessels in the eye.{{Cite web |date=2006-05-19 |title=Cytochalasin E |url=http://www.eyesight.org/Research/Research-Cytochalasin_E/research-cytochalasin_e.html |access-date=2022-05-12 |website= |archive-url=https://web.archive.org/web/20060519050124/http://www.eyesight.org/Research/Research-Cytochalasin_E/research-cytochalasin_e.html |archive-date=19 May 2006 |url-status=dead}}

Cytochalasin E was found to be a potent and selective inhibitor of bovine capillary endothelial (BCE) cell proliferation. Cytochalasin E differs from other cytochalasin molecules by having an epoxide, which is required for specificity and potency. Cytochalasin E is a potent antiangiogenic agent that may be useful for treatments of cancer and other pathologic angiogenesis.{{Cite journal |last1=Udagawa |first1=T. |last2=Yuan |first2=J. |last3=Panigrahy |first3=D. |last4=Chang |first4=Y. H. |last5=Shah |first5=J. |last6=D'Amato |first6=R. J. |date=2000-08-01 |title=Cytochalasin E, an epoxide containing Aspergillus-derived fungal metabolite, inhibits angiogenesis and tumor growth |url=https://pubmed.ncbi.nlm.nih.gov/10900214/ |journal=The Journal of Pharmacology and Experimental Therapeutics |volume=294 |issue=2 |pages=421–427 |issn=0022-3565 |pmid=10900214}} Cytochalasin E was also found to inhibit autophagy, a process vital in recycling dysfunctional cells and cellular components. Cancer cells thus favor autophagy due to its role in countering metabolic stresses induced by anti-cancer drugs such as bortezomib in order to regenerate healthier cancer cells for continued proliferation and growth. In a study, it was confirmed that when CE was used, fusion of autophagosomes with lysozyme was inhibited and so cell death due to bortezomib, a proteasome inhibitor, was amplified as unnecessary proteins would continue to build up inside cancer cells unable to be further recycled through autophagy, leading to apoptosis.{{Cite journal |last1=Takanezawa |first1=Yasukazu |last2=Nakamura |first2=Ryosuke |last3=Kojima |first3=Yuka |last4=Sone |first4=Yuka |last5=Uraguchi |first5=Shimpei |last6=Kiyono |first6=Masako |date=2018-04-06 |title=Cytochalasin E increased the sensitivity of human lung cancer A549 cells to bortezomib via inhibition of autophagy |url=https://pubmed.ncbi.nlm.nih.gov/29524420/ |journal=Biochemical and Biophysical Research Communications |volume=498 |issue=3 |pages=603–608 |doi=10.1016/j.bbrc.2018.03.029 |issn=1090-2104 |pmid=29524420}}