Hesperadin

Hesperadin
Names
	Preferred IUPAC name N-[(3Z)-2-Oxo-3-(phenyl{4-[(piperidin-1-yl)methyl]anilino}methylidene)-2,3-dihydro-1H-indol-5-yl]ethanesulfonamide
Identifiers
CAS Number	422513-13-1 ;
3D model (JSmol)	Interactive image;
ChemSpider	8318096 ;
PubChem CID	10142586;
UNII	PTR491OS14 ;
CompTox Dashboard (EPA)	DTXSID00195086 ;
	InChI InChI=1S/C29H32N4O3S/c1-2-37(35,36)32-24-15-16-26-25(19-24)27(29(34)31-26)28(22-9-5-3-6-10-22)30-23-13-11-21(12-14-23)20-33-17-7-4-8-18-33/h3,5-6,9-16,19,30,32H,2,4,7-8,17-18,20H2,1H3,(H,31,34)/b28-27- Key: GLDSKRNGVVYJAB-DQSJHHFOSA-N ; InChI=1/C29H32N4O3S/c1-2-37(35,36)32-24-15-16-26-25(19-24)27(29(34)31-26)28(22-9-5-3-6-10-22)30-23-13-11-21(12-14-23)20-33-17-7-4-8-18-33/h3,5-6,9-16,19,30,32H,2,4,7-8,17-18,20H2,1H3,(H,31,34)/b28-27- Key: GLDSKRNGVVYJAB-DQSJHHFOBF;
	SMILES CCS(=O)(=O)NC1=CC2=C(C=C1)NC(=O)C2=C(C3=CC=CC=C3)NC4=CC=C(C=C4)CN5CCCCC5;
Properties
Chemical formula	C29H32N4O3S
Molar mass	516.66 g·mol−1
	Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
	(what is ?)
	Infobox references

Hesperadin is an aurora kinase inhibitor.

The small molecule inhibits chromosome alignment and segregation by limiting the function of mitotic kinases Aurora B and Aurora A. Hesperadin causes cells to enter anaphase much faster, sometimes before the chromosomes are properly mono-oriented.^[1]

Hesperadin, like other miotic inhibitors, limits and sometimes can stop the process of mitosis in cells. For this reason, some have considered hesperadin's potential as a cancer-preventing drug.^[2]

Hesperadin works as an inhibitor, attaching to the active sites of Aurora A and Aurora B kinases.^[2]

References[]

^ Hauf, Silke; Cole, Richard W.; LaTerra, Sabrina; Zimmer, Christine; Schnapp, Gisela; Walter, Rainer; Heckel, Armin; van Meel, Jacques; Rieder, Conly L. (2003-04-28). "The small molecule Hesperadin reveals a role for Aurora B in correcting kinetochore-microtubule attachment and in maintaining the spindle assembly checkpoint". The Journal of Cell Biology. 161 (2): 281–294. doi:10.1083/jcb.200208092. ISSN 0021-9525. PMC 2172906. PMID 12707311.
^ ^a ^b Jetton, Neal; Rothberg, Karen G.; Hubbard, James G.; Wise, John; Li, Yan; Ball, Haydn L.; Ruben, Larry (April 2009). "The cell cycle as a therapeutic target againstTrypanosoma brucei: Hesperadin inhibits Aurora kinase-1 and blocks mitotic progression in bloodstream forms". Molecular Microbiology. 72 (2): 442–458. doi:10.1111/j.1365-2958.2009.06657.x. ISSN 0950-382X. PMC 2697958. PMID 19320832.

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[1] Hauf, Silke; Cole, Richard W.; LaTerra, Sabrina; Zimmer, Christine; Schnapp, Gisela; Walter, Rainer; Heckel, Armin; van Meel, Jacques; Rieder, Conly L. (2003-04-28). "The small molecule Hesperadin reveals a role for Aurora B in correcting kinetochore-microtubule attachment and in maintaining the spindle assembly checkpoint". The Journal of Cell Biology. 161 (2): 281–294. doi:10.1083/jcb.200208092. ISSN 0021-9525. PMC 2172906. PMID 12707311.

[Jetton-2] Jetton, Neal; Rothberg, Karen G.; Hubbard, James G.; Wise, John; Li, Yan; Ball, Haydn L.; Ruben, Larry (April 2009). "The cell cycle as a therapeutic target againstTrypanosoma brucei: Hesperadin inhibits Aurora kinase-1 and blocks mitotic progression in bloodstream forms". Molecular Microbiology. 72 (2): 442–458. doi:10.1111/j.1365-2958.2009.06657.x. ISSN 0950-382X. PMC 2697958. PMID 19320832.

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