Buparlisib (BKM120)

For research use only. Not for use in humans.

目录号：S2247 别名： NVP-BKM120

Molecular Weight(MW): 410.39

Buparlisib (BKM120, NVP-BKM120) 是一种选择性 PI3K 抑制剂，在无细胞试验中作用于p110α/β/δ/γ的IC50分别为 52 nM/166 nM/116 nM/262 nM。对 VPS34，mTOR，DNAPK 的作用效果下降，而对 PI4Kβ几乎没有活性。Buparlisib 可诱导凋亡。Phase 2。

规格

价格

库存

购买数量

10mM (1mL in DMSO)	RMB 2227.95	现货
5mg	RMB 1400.12	现货
10mg	RMB 2607.65	现货
50mg	RMB 7928.28	现货
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客户使用Selleck生产的Buparlisib (BKM120)发表文献153篇：

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J Exp Med, 2018, 215(1):159-175

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Nat Commun, 2017, 8:15623

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Proc Natl Acad Sci U S A, 2017, 114(41):E8628-E8636

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University Gattingen, 2013, Elisabeth Hand

PubMed: ( click the link to review the publication )

产品安全说明书

PI3K抑制剂选择性比较

生物活性

产品描述

特性

BKM120是可用于口服的生物有效的PI3K抑制剂。

靶点

p110α ^[1] (Cell-free assay)	p110δ ^[1] (Cell-free assay)	p110β ^[1] (Cell-free assay)	p110γ ^[1] (Cell-free assay)	Vps34 ^[1] (Cell-free assay)	点击更多
52 nM	116 nM	166 nM	262 nM	2.4 μM	点击更多

体外研究

BKM120作用于解除PI3K调节的细胞系，包括A2780, U87MG, MCF7和DU145时，具有抗增殖活性，GI50为0.1-0.7 nM。^[1] BKM120诱导多发性骨髓瘤细胞(ARP1, ARK, MM.1S, MM1.R和U266)凋亡，导致G1期细胞增多，S期细胞减少。BKM120诱导CD138+原代MM 细胞凋亡，且作用于CD138−基质细胞时毒性较低。BKM120可引起BimS的上调和XIAP的下调。^[2]BKM120作用于人类胃癌细胞系，降低mTOR下游信号，具有抗增殖活性。BKM120作用于KRAS突变的胃癌细胞系，可以增强p-ERK或 p-STAT3。BKM120 和STAT3阻断剂联用, 作用于含突变KRAS的细胞，诱导凋亡，具有协同效应，但是作用于KRAS野生型细胞没有这种效果。^[3]BKM120主要通过Aurora B激酶调节有丝分裂崩坏。^[4]

Cell Data

Cell Lines	Assay Type	Concentration	Incubation Time	Formulation	Activity Description	PMID
MCF7	MUDDfZRwfG:6aXOgRZN{[Xl?		MYW3NkBp	NGThTmVFVVOR	M2XjemN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG1ETjdiY3XscJMh\XiycnXzd4lv\yCSSUPLZYxxcGFiRUW0OWshdXW2YX70JJdqfGhiR1m1NEBw\iByLkCwNFE2QCEQvF2=	NXOyNFlZOjR7MECyOlY>
DU145	MWDDfZRwfG:6aXOgRZN{[Xl?		MoHlO\|IhcA>?	MVPEUXNQ	NW\nb3RIS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hTFVzNEWgZ4VtdHNiZYjwdoV{e2mwZzDMT2IyKG23dHHueEB4cXSqIFfJOVAhd2ZiMD6wNFA1OzVizszN	MlTjNlQ6ODB{Nk[=
A2780	M2rsNGN6fG:2b4jpZ{BCe3OjeR?=		MoPEO\|IhcA>?	NIfnZllFVVOR	NYHaUGhuS3m2b4TvfIlkcXS7IHHnZYlve3RiUGTFUk1l\W[rY3nlcpQhcHWvYX6gRVI4QDBiY3XscJMhf2m2aDDHTVUxKG:oIECuNFAxPjN3IN88US=>	NGL3d4czPDlyMEK2Oi=>
U87MG	NEH0Z5FEgXSxdH;4bYMhSXO\|YYm=		NXz3cVhsPzJiaB?=	MnvWSG1UVw>?	MkTmR5l1d3SxeHnjbZR6KGGpYXnud5QhWFSHTj3k[YZq[2mnboSgbJVu[W5iVUi3UWch[2WubIOge4l1cCCJSUWwJI9nKDBwMECwOlk5KM7:TR?=	MVGyOFkxODJ4Nh?=
A2780	MlT0SpVv[3Srb36gRZN{[Xl?		M4TDNVEhcA>?	MX7EUXNQ	MkLrTY5pcWKrdHnvckBw\iCSSUPLMY1m\GmjdHXkJGFMXCCVZYK0O\|MheGixc4Doc5J6dGG2aX;uJJdqfGhiRVO1NEBw\iByLkC1OUDPxE1?	M3PMXVI1QTByMk[2
DU145	MUDGeY5kfGmxbjDBd5NigQ>?		M1v3XVEhcA>?	MnXVSG1UVw>?	NYPncHBLUW6qaXLpeIlwdiCxZjDQTVNMNW2nZHnheIVlKEGNVDDT[ZI1PzNicHjvd5Bpd3K7bHH0bY9vKGmwIHj1cYFvKESXMUS1JINmdGy\|IHjhdoJwemmwZzDMT2IyKG23dHH0bY9vKHerdHigSWM2OCCxZjCwMlA4OyEQvF2=	MnzzNlQ6ODB{Nk[=
A2780	NGTscIhHfW6ldHnvckBCe3OjeR?=		MVqxJIg>	NILJOmpFVVOR	M2TU[mlvcGmkaYTpc44hd2ZiUFmzT{1u\WSrYYTl[EBCU1RiU3XyOFc{KHCqb4PwbI9zgWyjdHnvckBqdiCSVFXOMYRm\mmlaXXueEBpfW2jbjDBNlc5OCClZXzsd{B4cXSqIFXDOVAhd2ZiMD6wO\|Qh\|ryP	NX7HV3k3OjR7MECyOlY>
MCF7	NXW4O4Q2TnWwY4Tpc44hSXO\|YYm=		NUDXVWd3OSCq	Mn;xSG1UVw>?	MYLJcohq[mm2aX;uJI9nKFCLM1vhcJBp[SCHNUS1T{BufXSjboStcYVlcWG2ZXSgRWtVKFOnckS3N{BxcG:\|cHjvdplt[XSrb36ge4l1cCCHQ{WwJI9nKDBwMTFOwG0>	MVqyOFkxODJ4Nh?=
U87MG	M1nYOGZ2dmO2aX;uJGF{e2G7		Mln2NUBp	MXXEUXNQ	NWDZ[ItSUW6qaXLpeIlwdiCxZjDQTVNMNW2nZHnheIVlKEGNVDDT[ZI1PzNicHjvd5Bpd3K7bHH0bY9vKGmwIGDUSW4u\GWoaXPp[Y51KGi3bXHuJHU5P02JIHPlcIx{KHerdHigSWM2OCCxZjCwMlE{KM7:TR?=	NYLzdmpuOjR7MECyOlY>
A2780	MmK4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?		NXXQbWdLPzJiaB?=	NX\1fIU5TE2VTx?=	MkXLSWM2OD1yLkWyJO69VQ>?	M{HOTFI1QTByMk[2
SKMES-1	NUnO[GtMS3m2b4TvfIlkKEG\|c3H5	MVmxJO69VQ>?	MX:3NkBp		NXTQbFYxUW6mdXPld{Bk\WyuIHTlZZRp	MojLNlYxOTN\|MUi=
H596	NFe3dZVHfW6ldHnvckBCe3OjeR?=	NHrI[JkyKM7:TR?=			NFvPfJJKdXCjaYLzJINmdGxibXnndoF1cW:w	Ml23NlYxOTN\|MUi=
HCC2450	M4DNXmZ2dmO2aX;uJGF{e2G7	NUn1U2E4OSEQvF2=			MXjJcZBicXK\|IHPlcIwhcW64YYPpc44>	MYiyOlAyOzNzOB?=
A549	NGfofHZHfW6ldHnvckBCe3OjeR?=	NFvXTo42ODBibl2=	MnPpOFghcA>?	Mni1SG1UVw>?	MXzJcohq[mm2czDBb5Qh[WO2aY\heIlwdg>?	MlLrNlU6Ozd{OUm=
A549	MVnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NU\FXlM1OSEQvF2=	MYi3NkBp	NGSzWo5FVVOR	M2LXdWlvcGmkaYTzJINmdGxiZ4Lve5Rp	MWmyOVk{PzJ7OR?=
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H1975	MoTtS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NHvN[lkxNjNvOT62{txO	M37vPVczcA>?	NV;3fIN6TE2VTx?=	M1LoOGlEPTB;MT6zPFXPxE1?	NFLOc4szPDN\|N{i0Oi=>
H1975	MWDBdI9xfG:\|aYOgRZN{[Xl?	NXTtdZBMOs7:TR?=	MV:yOIg>	M2LCRmROW09?	MofHbY5kemWjc3XzJIFxd3C2b4Ppd{Bz[XSnIIPp[45q\mmlYX70cJk>	MX2yOFM{Pzh2Nh?=
T-ALL	NUPIbI52SXCxcITvd4l{KEG\|c3H5	MmDIZoV1f2WnbjCxMlQh[W6mIEWuN{BuVSCjdDCyOIgh[W6mIECuPUBidmRiNT61JI1OKGG2IES4bEBqdiCmaX\m[ZJmdnRiY3XscEBtcW6n	MnLMNlQhd3JiNEjo	NEOycFNFVVOR	NIXDdYZi\m[nY4TzJJRp\SCSSUPLJJBifGi5YYmgbY4hXC2DTFygZ4VtdCCuaX7ldy=>	M4nTcFI1OzFyN{O2
BCR-ABL	MoTaS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NVXKc2lvOC5{NT2xNO69VQ>?	MX[0[C=>		M4XjdpNq\26rZnnjZY51dHliaX7obYJqfCClZXzsJJBzd2yrZnXyZZRqd25?	MXqyOFI1PDZzMh?=
LC-1/SQSF	NEHWZWdHfW6ldHnvckBCe3OjeR?=	NWLTeVhmO87:TR?=	M4K4dlI1cA>?	NGS2bYNFVVOR	NEPBUpRl\WO{ZXHz[UBPWkZ{IIDyc5RmcW5ibHX2[Yw>	NGHa[FAzOzl6MEC5Ny=>
Primary CLL cells	M4LnRmFxd3C2b4Ppd{BCe3OjeR?=	NIP3boQyNTFyzszN	NW\4d5J3PDiq		MYDpcoR2[2W\|IHHwc5B1d3OrczDpckBEVExiY3XscJMhcW6mZYDlcoRmdnRib3[gdJJw\26xc4TpZ{Bu[XKtZYLz	NHfFXoczOzh3MEiwOy=>
Primary CLL cells	NXT5ZXhqU2mwYYPlJGF{e2G7	MoXQNu69VQ>?	M4CwfFMxdWmw		MoTB[IVkemWjc3XkJHBKO0tiYXP0bZZqfHl?	NUfQeXoyOjN6NUC4NFc>
Primary CLL cells	NXv5S2p4S3m2b4TvfIlkKEG\|c3H5	MoPJNu69VQ>?	M4\BPFI1cA>?		NYTrbHpPcW6mdXPld{Bk\WyuIHP5eI91d3irY3n0fS=>	NYS5V\|k5OjN6NUC4NFc>
human NSCLC cell lines	MlnSRZBweHSxc3nzJGF{e2G7	NIfJO5cxNjF{NT20{txO	Mm\INlRp	MYjEUXNQ	NWT1N2NxUUN3MIOgdoFv\2W\|IH\yc40hOC52LUNOwG0>	MWWyN\|U3OjR5Mh?=
human HCC cell lines	NIjZeVVE\WyuII\pZYJqdGm2eTDhd5NigQ>?	NWjWdnZZOC5yMEWtNe69VQ>?	M3\mdVQ5cA>?		M2PKNWlEPTB;Md88US=>	MYmyN\|Q5QTl7OR?=
Huh7	NVrRe4N6U2mwYYPlJGF{e2G7	NIPj[\|My\|ryP	NIjNblY1QGh?		MnPHd4lodmoxrJHjZY51dHlicnXkeYNmeyCyaH;zdIhwenmuYYTpc44hd2ZiQXv0	MW[yN\|Q5QTl7OR?=
SK-HEP1	NVTqXWhpT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	M4nET\|EuOjEQvF2=	MUS3Nog>	NF7lbmdFVVOR	NYWyblVUUUN3MP-8oFHPxE1?	MYGyN\|Q4QTF\|Nh?=
786-0	M4HsZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NGnhbZoyNTJyzszN	M3jxUlczcA>?	NUL1NXhnTE2VTx?=	M4jadWlEPTExvKyx{txO	NGLoOmwzOzR5OUGzOi=>
JVM2	M{P3WWN6fG:2b4jpZ4l1gSCjc4PhfS=>	MXuwMlIuOjEQvF2=	Ml7XO\|Jp	MUfEUXNQ	Mlq1TWM2OD1yLkpOwG0>	MoD2NlMzOzh4M{m=
EHEB	NYTBS2xiS3m2b4TvfIlkcXS7IHHzd4F6	MV:wMlIuOjEQvF2=	MYO3Nog>	NXnHWFl{TE2VTx?=	Mn32TWM2OD1yLkhOwG0>	NH[zSZYzOzJ\|OE[zPS=>
MEC2	M4PuRWN6fG:2b4jpZ4l1gSCjc4PhfS=>	M2\kZ\|AvOi1{MN88US=>	NF3Ycng4Omh?	NXTZZVdDTE2VTx?=	NYrMbnpvUUN3ME2wMlfPxE1?	M3Kxe\|I{OjN6NkO5
primary B-CLL lymphocytes	Mkf3RZBweHSxc3nzJGF{e2G7	NFP1cWpKSzVyIH\vdkBm[WOqIIDybY1ienliY3XscEBtcW6n	Mnf5NlRp	MXrEUXNQ	MYXJR\|Ux97zeM988UUBnd3JiYXzsJJBifGmnboTz	MViyN\|I{QDZ\|OR?=
primary B-CLL lymphocytes	M2O0cmtqdmG\|ZTDBd5NigQ>?	NXXwbpRNUUN3MDDmc5Ih\WGlaDDwdolu[XK7IHPlcIwhdGmwZR?=	MVKyOIg>		NVuzfld{cW6qaXLpeJMheDdyU{\LJEYhPEVvQmCxJIV5eHKnc4Ppc44>	MWSyN\|I{QDZ\|OR?=
human NSCLC	NULhZmc4T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	M130[VAvPS1{zszN	MWK3Nog>		NX7GOVNxUUN3ME2x{txO	Mm\pNlI4QDF\|OUO=
human NSCLC	M1vYO2tqdmG\|ZTDBd5NigQ>?	Ml:yNe69VQ>?	NYXBSoZPOjSq		NHnHSIVqdmirYnn0d{B1cGViQXv0M41VV1Jic3nncoFtcW6pIIDheIh4[XliYYSgN4gh[W[2ZYKgeJJm[XSvZX70	MmPWNlI4QDF\|OUO=
Y1 cell line	Mo\WS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	MVewMlHPxE1xMd88US=>	Ml\6NlRp	NGXVVYxFVVOR	NUXPU5RtcW6qaXLpeJMhPjExvJWgZ4VtdCC4aXHibYxqfHliaX6gUZlkNVOldIKteJJidnOoZXP0[YQh[2WubIO=	MoHJNlI3QTJ7MES=
PIK3CA-mutant MCF7	NYflR2N4T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NGT3[WZIUTVyPUG2NOKyQTGwTf-8kGxFPTB;OUiwxtEzPzOwTR?=	MVK3Nog>		NVLvNJlZT0l3ME2xOlDDuTlzbl5vwKxNTDVyPUm4NOKyOjd\|bl2=	M3TQdFIzPjV\|OU[3
PIK3CA-mutant MCF7	Ml;lT4lv[XOnIFHzd4F6	MlWxTWM2OD1zMUVCtVNvVQ>?	Mn3tO\|Jp		NEjvb5FKSzVyPUGxOOKyO26PIHnuJJJm\HWlaX7nJGFsfCCyaH;zdIhwenmuYYTpc44hdGW4ZXzz	M4DXXlIzPjV\|OU[3
MCF7-myr-Akt	MnXRS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NH:wUGdIUTVyPUK5PeKyPjiwTf-8kGxFPTExvK6xNEwxODCwTR?=	NH\GZpo4Omh?		NH23elhIUTVyPUK5PeKyPjiwTf-8kGxFPTExvK6xNEwxODCwTR?=	M4Szd\|IzPjV\|OU[3
colon cancer cell lines	MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MnL6NE0yOM7:TR?=	MXq3Nog>	MWXEUXNQ	MlmwTWM2OD1zzszN	NHjZeZkzOjV2M{i1Oy=>
gastric cancer cell lines	NGG4e4dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	Mom2NE0yOM7:TR?=	NIP5TJY4Omh?	Ml\CSG1UVw>?	M2[5WWlEPTB;Mj21{txO	NWXaXFV[OjJ3NEO4OVc>
HCT-116/HT-29/MKN-45	MWXBdI9xfG:\|aYOgRZN{[Xl?	NGqzO5kz\|ryP	MUm0PIg>		NIDoRZd{cGmodDDpckBIOiCyaHHz[S=>	MVSyNlU1Ozh3Nx?=
HT-29 and HCT-116	MYXDZZNx[XOnIHHzd4F6	MoW2Oe69VQ>?	NXX1NVM2OjSq		NEjWWnNqdmS3Y3XzJINie3Cjc3WgZYN1cX[rdIm=	NYeyO4E2OjJ3NEO4OVc>
MM cell lines	MljCS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	M{LPT\|Ex\|ryP	NVjxVYpiOjSq	MkDUSG1UVw>?	MnzyTWM2OCC4YYLp[ZMh[W2xbneg[Iln\mW{ZX70JINmdGxibHnu[ZMhcW5idHnt[UBidmRiZH;z[UBl\XCnbnTlcoNm	NVfBRWozOjJ{MEe0PFU>
ARP-1	NHLoNVRCeG:ydH;zbZMhSXO\|YYm=	M{fJXFEx\|ryP	NFzxcVUzPGh?	M3T5XmROW09?	MYnpcoR2[2W\|IF3NJINmdGxiYYDvdJRwe2m\|IITodo92\2hiY3HzdIF{\SCjY4TpeoF1cW:w	NI\rfngzOjJyN{S4OS=>
SNU-601	MmD3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?		MXK3Nog>	Moj0SG1UVw>?	MU\JR\|UxRTBwOEG2xtExNjB4M988US=>	MV6yNlE2QThzNB?=
SNU-1	MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?		M2LiXVczcA>?	Mn70SG1UVw>?	MlnTTWM2OD1zLkC4NuKyOC5yMklOwG0>	MmixNlIyPTl6MUS=
SNU-668	MVPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?		MWW3Nog>	NWLhRYdxTE2VTx?=	MWjJR\|UxRTFwNUe5xtExNjB5NN88US=>	Mn:4NlIyPTl6MUS=
AGS	M{jWWGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7		M{nkblczcA>?	NVXnfI5kTE2VTx?=	NXHXRZpDUUN3ME2xMlcyPMLzMD6xNVfPxE1?	NWjqbotOOjJzNUm4NVQ>
SNU-216	M3nYNmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7		NIf2fVY4Omh?	NYXXTZhNTE2VTx?=	MXHJR\|UxRTJwNkmyxtExNjB6Mt88US=>	NX7vc5lQOjJzNUm4NVQ>
SNU-5	MVvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?		MlTCO\|Jp	NFzrXnZFVVOR	M4jCd2lEPTB;MT6zOVHDuTBwMEmx{txO	NELjZoYzOjF3OUixOC=>
SNU-638	NX;wdHg{T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=		NUD5dWV6PzKq	MW\EUXNQ	Ml31TWM2OD1{LkK4NuKyOC5yNUROwG0>	Ml3CNlIyPTl6MUS=
SNU-16	M3j6UWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7		MXO3Nog>	MYfEUXNQ	NVnYeoRQUUN3ME2xMlU4O8LzMD6wNFHPxE1?	NEmyZnkzOjF3OUixOC=>
SNU-484	M4jFfGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7		M1nGZlczcA>?	NGS2fWZFVVOR	NHLUc25KSzVyPUGuO\|I5yrFyLkC0Oe69VQ>?	MojsNlIyPTl6MUS=
SNU-620	M3XP[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7		M1vOPFczcA>?	NXXhSFJ3TE2VTx?=	NHnEcYxKSzVyPUKuPVM6yrFyLkCwNe69VQ>?	MVWyNlE2QThzNB?=
SNU-719	MWTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?		MVe3Nog>	NFzSUINFVVOR	MV\JR\|UxRTNwMEO3xtExNjB\|Mt88US=>	M2O5N\|IzOTV7OEG0
glioma cell lines	NFL6XHFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=		MYG3Nog>		M3TKTWlEPTB;MT2y{txO	M3[yd\|IzODZ3MEiw
U87	MnfJRZBweHSxc3nzJGF{e2G7	MoXvNu69VQ>?	MYe3Nog>		NH3mZ2ZqdmS3Y3XzJINmdGxiYYDvdJRwe2m\|IHHu[EBkdGWjdnXkJHBCWlBiYX7kJINie3Cjc3WtNy=>	M2j6[lIzODZ3MEiw

... Click to View More Cell Line Experimental Data

Assay

Methods	Test Index	PMID
Western blot	p-AKT (T308) / p-AKT (S473) / AKT; PubMed: 27283525 J Neurooncol Left western blots showing levels of pAkt (T308), pAkt (S473) and total Akt in U87 cells exposed to buparlisib for 72 h. Right densitometric assessment of western blots, showing relative changes in phosphorylation. p-FOXO3a (S253) / FOXO3a; PubMed: 28036259 Oncotarget Cells were treated with 0.5 μM BKM120 for 24 h and cell lysates were immunoblotted with the indicated antibodies. Actin was used as the loading control. Nuclear NF-κB p65 / NF-κB p65; PubMed: 26673665 Cell Death Dis Western blots show BKM120 downregulating pAKT, nuclear NF-κB p65 and total NF-κB p65 in MDR and their parental cells. β-actin was used as a loading control for pAKT, AKT and total NF-κB p65. Lamin B was used as a loading control for nuclear NF-κB p65. p-ERK / ERK / LC3; PubMed: 27572309 Oncotarget The indicated cell lines were exposed to different concentrations of BKM120 as indicated for 8 h A. or with 2 μM BKM120 for the indicated times B. The cells were then harvested for preparation of whole-cell protein lysates and subsequent Western blot analysis to detect the given proteins. p-STAT3 / STAT3 / p-ERK / ERK / p-S6; PubMed: 29928341 Oncol Lett Western blot analysis of H460 and H2126 cell lysates using specific antibodies to phosphorylated or total proteins of STAT3, ERK1/2, AKT, S6 or GAPDH (loading control). The cells were treated with increasing concentrations of BKM120 for 24 h. p-MET / MET; PubMed: 29928341 Oncol Lett The expression of phosphorylated or total forms of MET protein was analyzed by western blotting.	27283525 28036259 26673665 27572309 29928341
Immunofluorescence	FOXO3a; PubMed: 28036259 Oncotarget Cells were cultured on coverslips to approximately 60% confluency and then treated with 1 μM BKM120 for an additional 24 h. Immunofluorescence staining was performed using an anti-FOXO3a antibody and the nuclei were stained with DAPI. Scale bar, 20 μm.	28036259
Growth inhibition assay	Cell viability; PubMed: 26673665 Cell Death Dis Dose-response curves were used to calculate the IC50 of BKM120 for MCs of MCF-7/A02 cells (upper) and CALDOX cells (lower).	26673665

体内研究

BKM120按30, 60, 或100 mg/kg剂量作用于A2780移植瘤，完全抑制pAKTser473。BKM120按 30和 60 mg/kg剂量作用于U87MG神经胶质瘤模型，显示抗癌活性。^[1]BKM120每天按5μM/kg剂量处理具有持久生命力的ARP1 SCID鼠模型，导致肿瘤体积和K链水平明显降低。^[2]

激酶实验：^[2]	- 合并 PI3K 生化实验(ATP 消耗实验): BKM120溶于DMSO中，按每孔1.25 µL直接加到黑色384孔板上。开始反应, 25 µL 10nM PI3K和5 µg/mL 1-α-磷酸肌醇(PI)加到实验 buffer (10 mM Tris pH 为7.5, 5 mM MgCl₂, 20 mM NaCl, 1 mM DTT，及0.05% CHAPS)，然后加到每孔中，随后在实验buffer中加入25 µL 2 µM ATP。反应进行直到50% ATP被消耗，然后加入25 µL KinaseGlo溶液终止反应。终止的反应温育5分钟，然后通过荧光测定残留的ATP。
细胞实验：^[1]	- 合并 Cell lines: A2780细胞 Concentrations: 0-6.6 μM Incubation Time: 3天 Method: A2780细胞培养在含10% FBS,L-谷氨酸,丙酮酸钠和抗生素的DMEM培养基上。细胞按每孔10³个细胞的密度接种在相同培养基上，温育3到5小时。稀释溶于20 mM DMSO中的BKM120。2 µL稀释的BKM120溶液加到细胞培养基上, (浓度为0-6.6 µM)。等体积(100 µL)溶液加到96孔板中，在37^oC下温育3天。使用Trilux读取荧光值而测定抑制细胞增殖的效果 (Only for Reference)
动物实验：^[1]	- 合并 Animal Models: 携带U87MG 和A2780移植瘤的雌性裸鼠 Dosages: ~60 mg/kg Administration: 每天口服处理 (Only for Reference)

参考文献

[4] Koul D, et al. Clin Cancer Res, 2012, 18(1), 184-195.

- 合并

溶解度 (25°C)

体外	DMSO	82 mg/mL (199.8 mM)
	Water	Insoluble
	Ethanol	'2 mg/mL
体内	从左到右依次将纯溶剂加入产品，现配现用(数据来自Selleck实验检测而非文献)： 5% DMSO+30% PEG 300+ddH2O	15mg/mL

* 溶解度检测是由Selleck技术部门检测的，可能会和文献中提供的溶解度有所差异，这是由于生产工艺和批次不同产生的正常现象。请按照顺序依次加入各个纯溶剂。

化学数据 Download Buparlisib (BKM120) SDF

分子量	410.39
化学式	C₁₈H₂₁F₃N₆O₂
CAS号	944396-07-0
储存条件	3年-20°C 粉状 2年-80°C 溶于溶剂
别名	NVP-BKM120

动物体内配方计算器 (澄清溶液)

第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量）

给药剂量

mg/kg

动物平均体重

每只动物给药体积

动物数量

只

第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系Selleck为您提供正确的澄清溶液配方）

% DMSO+ % + % Tween 80+ % ddH₂O

计算重置

计算结果:

工作液浓度： mg/ml；

DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，注：如该浓度超过该批次药物DMSO溶解度，请先联系Selleck）；

体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL ddH₂O，混匀澄清。

注意：1. 首先保证母液是澄清的；
2. 一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。

计算器

摩尔浓度计算器

本计算器可帮助您计算出特定溶液中溶质的质量、溶液浓度和体积之间的关系，公式为:

质量 (mg) = 浓度 (mM) x 体积 (mL) x 分子量 (g/mol)

摩尔浓度计算公式

质量

浓度

体积

分子量
=

×

×

*在配置溶液时，请务必参考Selleck产品标签上、MSDS / COA（可在Selleck的产品页面获得）批次特异的分子量使用本工具。

稀释计算器

用本工具协助配置特定浓度的溶液，使用的计算公式为：

开始浓度 x 开始体积 = 最终浓度 x 最终体积

稀释公式

稀释公式一般简略地表示为: C1V1 = C2V2 ( 输入输出 )

C1

V1

C2

V2
×

=

×

在配置溶液时，请务必参考Selleck产品标签上、MSDS / COA（可在Selleck的产品页面获得）批次特异的分子量使用本工具。.

连续稀释计算器方程

连续稀释
初始浓度:
稀释倍数:

计算结果

C1=C0/X	C1:	LOG(C1):
C2=C1/X	C2:	LOG(C2):
C3=C2/X	C3:	LOG(C3):
C4=C3/X	C4:	LOG(C4):
C5=C4/X	C5:	LOG(C5):
C6=C5/X	C6:	LOG(C6):
C7=C6/X	C7:	LOG(C7):
C8=C7/X	C8:	LOG(C8):

分子量计算器

通过输入化合物的化学式来计算其分子量：

注：化学分子式大小写敏感。C10H16N2O2 c10h16n2o2

摩尔浓度计算器

质量	浓度	体积	分子量
=	×	×
计算

临床试验信息 (data from https://clinicaltrials.gov, updated on 2020-05-15)

NCT Number	Recruitment	interventions	Conditions	Sponsor/Collaborators	Start Date	Phases
NCT04338399	Not yet recruiting	Drug: Buparlisib & Paclitaxel	Head and Neck Cancer	Adlai Nortye Biopharma Co. Ltd.	July 31 2020	Phase 3
NCT02614508	Terminated	Drug: Buparlisib\|Drug: Ibrutinib\|Biological: Ofatumumab	Recurrent Chronic Lymphocytic Leukemia\|Recurrent Small Lymphocytic Lymphoma\|Refractory Chronic Lymphocytic Leukemia\|Refractory Small Lymphocytic Lymphoma	Emory University\|Novartis	January 2016	Phase 1
NCT01613677	Withdrawn	Drug: BKM120	Treatment for Metastatic or Locally Advanced Cervical Cancer	Novartis Pharmaceuticals\|Novartis	November 2015	Phase 2

技术支持

在订购、运输、储存和使用我们的产品的任何阶段，您遇到的任何问题，均可以通过拨打我们的热线电话400-668-6834，或者技术支持邮箱tech@selleck.cn，直接联系到我们。我们会在24小时内尽快联系您。

操作手册

如果有其他问题，请给我们留言。

PI3K Signaling Pathway Map

PI3K Inhibitors with Unique Features

选择性强的PI3K抑制剂

CAL-101 (Idelalisib, GS-1101) : p110δ-selective, IC50=2.5 nM.
选择性强的PI3K抑制剂

TGX-221 : p110β-specific, IC50=5 nM.
活性最高的PI3K抑制剂

BEZ235 (NVP-BEZ235, Dactolisib) : p110α/γ/δ/β, IC50=4 nM/5 nM/7 nM/75 nM.
FDA批准的PI3K抑制剂

CAL-101 (Idelalisib, GS-1101) : Approved by FDA for Relapsed Chronic Lymphocytic Leukemia, Follicular Lymphoma and Small Lymphocytic Lymphoma.
最新的PI3K抑制剂

VS-5584 (SB2343) ^New : Potent and selective dual PI3K/mTOR inhibitor for mTOR, PI3Kα/β/δ/γ with IC50 of 3.4 nM and 2.6-21 nM, respectively.

研究领域

产品类型

Buparlisib (BKM120)

客户使用Selleck生产的Buparlisib (BKM120)发表文献153篇：

产品安全说明书

PI3K抑制剂选择性比较

生物活性

推荐的实验操作(此推荐来自于公开的文献所以Selleck并不保证其有效性)

参考文献

溶解度 (25°C)

化学数据 Download Buparlisib (BKM120) SDF

动物体内配方计算器 (澄清溶液)

计算器

摩尔浓度计算器

质量 (mg) = 浓度 (mM) x 体积 (mL) x 分子量 (g/mol)

摩尔浓度计算公式

稀释计算器

开始浓度 x 开始体积 = 最终浓度 x 最终体积

稀释公式

连续稀释计算器方程

连续稀释

计算结果

分子量计算器

总分子量：g/mol

摩尔浓度计算器

临床试验信息 (data from https://clinicaltrials.gov, updated on 2020-05-15)

技术支持

PI3K Signaling Pathway Map

PI3K Inhibitors with Unique Features

相关PI3K产品