Capivasertib (AZD5363)

Catalog No.S8019

Capivasertib (AZD5363) Chemical Structure

Molecular Weight(MW): 428.92

AZD5363 potently inhibits all isoforms of Akt(Akt1/Akt2/Akt3) with IC50 of 3 nM/8 nM/8 nM in cell-free assays, similar to P70S6K/PKA and lower activity towards ROCK1/2. Phase 2.

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Cited by 29 Publications

Purity & Quality Control

Choose Selective Akt Inhibitors

Biological Activity

Description AZD5363 potently inhibits all isoforms of Akt(Akt1/Akt2/Akt3) with IC50 of 3 nM/8 nM/8 nM in cell-free assays, similar to P70S6K/PKA and lower activity towards ROCK1/2. Phase 2.
Features Moderate preclinical tolerability, and PD characteristics of an AKT inhibitor. Distinct profile from other AKT inhibitors in clinical development.
Targets
Akt1 [1]
(Cell-free assay)		 Akt2 [1]
(Cell-free assay)		 Akt3 [1]
(Cell-free assay)		 ROCK2 [1]
(Cell-free assay)
3 nM 8 nM 8 nM 56 nM
In vitro

AZD5363 is a potent Akt inhibitor with IC50 of 3 nM, 8 nM and 8 nM for Akt1, Akt2 and Akt3, respectively. [1] AZD5363 inhibits phosphorylation of AKT substrates in cells with a potency of approximately 0.3 to 0.8 μM. AZD5363 inhibits the proliferation of 41 of 182 solid and hematologic tumor cell lines with a potency of < 3 μM. [2] Activating mutations in PIK3CA, loss or inactivation of tumor suppressor PTEN, or HER2 amplification all are significantly predictive of responsiveness to AZD5363. Additionally, correlation is also seen between the RAS mutation status of cell lines and resistance to AZD5363. [1]
Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
MCF7 NFzUPVhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWiyNFAhdk1? NWLXco9pPiCm NXvn[GEzcW6lcnXhd4VlKGS{dXegd4Vve2m2aY\peJkhd2ZiND3PTHQh[W6mIH\1cJZme3S{YX70 NVW1Zm1NOjZ|NUGzNlM>
ZR75 M{joXWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4\4WVExOCCwTR?= MUK2JIQ> NFW1R3dqdmO{ZXHz[YQh\HK3ZzDz[Y5{cXSrdnn0fUBw\iB2LV;IWEBidmRiZoXseoV{fHKjboS= NGHuUVMzPjN3MUOyNy=>
T74D M1jCWWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXrkeGkxOTByIH7N NUDLRmdVPiCm NEThOG5qdmO{ZXHz[YQh\HK3ZzDz[Y5{cXSrdnn0fUBw\iB2LV;IWEBidmRiZoXseoV{fHKjboS= NXXPXW1JOjZ|NUGzNlM>
1%MCF7 MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXi0NFAhdk1? MW[2JIQ> MnTVbY5kemWjc3XkJIRzfWdic3Xud4l1cX[rdImgc4YhPC2RSGSgZY5lKG[3bI\ld5Rz[W62 NWfmO|Y2OjZ|NUGzNlM>
MCF7 LTED MWrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHPzd2czODBibl2= Mni2OkBl NXnEWINCcW6lcnXhd4VlKGS{dXegd4Vve2m2aY\peJkhd2ZiND3PTHQh[W6mIH\1cJZme3S{YX70 NY\wbHFuOjZ|NUGzNlM>
ZR75 LTED MXvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnrPNVAxKG6P MXq2JIQ> MXHpcoNz\WG|ZXSg[JJ2\yC|ZX7zbZRqfmm2eTDv[kA1NU:KVDDhcoQh\nWudnXzeJJidnR? MoHyNlY{PTF|MkO=
T74D LTED Ml;wS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWj1[|VqOTByIH7N NXHjTYFyPiCm NWHDTFJ{cW6lcnXhd4VlKGS{dXegd4Vve2m2aY\peJkhd2ZiND3PTHQh[W6mIH\1cJZme3S{YX70 NGe4Uo0zPjN3MUOyNy=>
TamR NGfOeJhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYW0NFAhdk1? M1rORVYh\A>? NGPucG5qdmO{ZXHz[YQh\HK3ZzDz[Y5{cXSrdnn0fUBw\iB2LV;IWEBidmRiZoXseoV{fHKjboS= MUeyOlM2OTN{Mx?=
HCC1954 NYXTPVRsT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkTNNE0yNjN3IN88US=> MlnuOUBl NYDnd4Zt\W6qYX7j[ZMhfGinIHfyc5d1cCCrbnjpZol1cW:wIH;mJGFbTDh7M{G= NHfofIIzPjB7NUS3OS=>
BT474c NVL1WG9YT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NITacHIxNTFwM{Wg{txO M4TafVUh\A>? MV7lcohidmOnczD0bIUh\3Kxd4ToJIlvcGmkaYTpc44hd2ZiQWrEPFk{OQ>? MX2yOlA6PTR5NR?=
KPL4 NVPiUoliT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIT3TpgxNTFwM{Wg{txO MlfROUBl MYTlcohidmOnczD0bIUh\3Kxd4ToJIlvcGmkaYTpc44hd2ZiQWrEPFk{OQ>? M3S3cVI3ODl3NEe1
SKBR3 NGrXXXdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmHpNE0yNjN3IN88US=> MYq1JIQ> NHj2SZRmdmijbnPld{B1cGViZ4Lve5RpKGmwaHnibZRqd25ib3[gRXpFQDl|MR?= NIPnN2szPjB7NUS3OS=>
MR49C NGr5ZVdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYHqVW53OC13IN88US=> Mn7ROFghcA>? NXjReINqcW6qaXLpeJMh[2WubDDndo94fGhiaX6gZUBld3OnIHTldIVv\GWwdDDtZY5v\XJ? NWHaUXhXOjVzNUGwNVI>
MR49F NIrnSGhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mni3NE02KM7:TR?= NF\xPYo1QCCq MYLpcohq[mm2czDj[YxtKGe{b4f0bEBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> M33uflI2OTVzMEGy
NCI-H522 NV\t[4hNT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3v4UWlEPTB;MUGuN{ApyrF{LkepJO69VQ>? M4rYXlI1QTV5Nkiy
PC-9 NI\FdFhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MY\JR|UxRTlwMzCoxtEyNjJrIN88US=> Mk[1NlQ6PTd4OEK=
NCI-H522 NF75bXJHfW6ldHnvckBCe3OjeR?= MXmxM|UwOTBizszN NXXXWGtRPC9{NDDo NWPuO5BpcW6lcnXhd4V{KEGNVDDwbI9{eGixconsZZRqd25? MnO0NlQ6PTd4OEK=
PC-9 MlTnSpVv[3Srb36gRZN{[Xl? NV\2eHVuOS93L{GwJO69VQ>? MlqxOE8zPCCq NHzT[ZRqdmO{ZXHz[ZMhSUuWIIDoc5NxcG:{eXzheIlwdg>? M33xelI1QTV5Nkiy
HGC27 MWTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1L1XGlEPTB;MD60OFUh|ryP NUXI[3RNOjRyOEizPFI>
IM95m M{nHemdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXTJR|UxRTBwNUGg{txO M2TUfVI1ODh6M{iy
AGS M1nm[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXvqU|Y5UUN3ME2wMlU2OiEQvF2= M1TDTFI1ODh6M{iy
NCI-N87 NGP4OJRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4naV2lEPTB;MT6wN|ch|ryP M{T1RlI1ODh6M{iy
23132/87 MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NY\lTWR7UUN3ME2xMlY4OSEQvF2= MmHuNlQxQDh|OEK=
MKN1 NEjQVI9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXzlfYN6UUN3ME2yMlQzOSEQvF2= Ml\RNlQxQDh|OEK=
SNU-620 NFv4O|lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnfrTWM2OD1|LkO4OEDPxE1? MlvFNlQxQDh|OEK=
SNU-638 NXT3VYZHT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIO2TldKSzVyPUSuOVI{KM7:TR?= NYTuRXZzOjRyOEizPFI>
SNU-1 MnHPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVrJR|UxRTVwMkW4JO69VQ>? NIG5fXozPDB6OEO4Ni=>
SNU-601 Ml3BS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYGxeJQ3UUN3ME21Mlk{QCEQvF2= MYSyOFA5QDN6Mh?=
SNU-668 MYjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWjJR|UxRTZwMECzJO69VQ>? Mo\NNlQxQDh|OEK=
HS746T Mki2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGfmXXBKSzVyPU[uNFg1KM7:TR?= M{\XeFI1ODh6M{iy
KATO III NUPSOXpOT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUfWOJF2UUN3ME23MlI3PyEQvF2= MWKyOFA5QDN6Mh?=
SNU-484 MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Ml\2TWM2OD15LkO5NkDPxE1? MWOyOFA5QDN6Mh?=
SNU-16 MlXPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUXJR|UxRTFzLkC5O{DPxE1? NUjzZ|BsOjRyOEizPFI>
OCUM-1 MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{Dw[WlEPTB;MUSuOVE2KM7:TR?= NHu0dGszPDB6OEO4Ni=>
NUGC-3 NWfTUIoyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFrhcXdKSzVyPUKxMlg4OyEQvF2= MXGyOFA5QDN6Mh?=
AZ521 NYDOZXd[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3W4dGlEPTB;MkWuOFQ5KM7:TR?= NUHrRlRiOjRyOEizPFI>
SNU-216 NXPBb2hGT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVfJR|UxRTNyIN88US=> NEPOfY0zPDB6OEO4Ni=>
NUGC-4 MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoHuTWM2OD1|MDFOwG0> MVOyOFA5QDN6Mh?=
SNU-5 NVzkeJNnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4fIZmlEPTB;M{Cg{txO MoHpNlQxQDh|OEK=
GTL-16 MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlziTWM2OD1|MDFOwG0> MlXINlQxQDh|OEK=
MKN74 MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnHNTWM2OD1|MDFOwG0> MlfONlQxQDh|OEK=
PAMC82 M{K1W2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXizdVVHUUN3ME2zNEDPxE1? NHHhWWczPDB6OEO4Ni=>
LNCaP MmjUSpVv[3Srb36gRZN{[Xl? M4CzcVUh|ryP NX3kUHBlOC1{NDDo M{Gwe4lv\HWlZYOgRWtVWzR5MzDhcoQhSUuWVEOwPEBxcG:|cHjvdplt[XSrb36gbY4h[SC2aX3lJIRmeGWwZHXueEBu[W6wZYK= Mm\FNlM6PjZ4MkG=
C4-2  NWHqVIlvTnWwY4Tpc44hSXO|YYm= MoTqOUDPxE1? NWHUWWtvOC1{NDDo NGe4OI9qdmS3Y3XzJGFMXFN2N{OgZY5lKEGNVGSzNFgheGixc4Doc5J6dGG2aX;uJIlvKGFidHnt[UBl\XCnbnTlcpQhdWGwbnXy NEjKRY0zOzl4Nk[yNS=>
LNCaP NWLuV5d4TnWwY4Tpc44hSXO|YYm= NXzFemlJPSEQvF2= NVz0SmlJOC1{NDDo Mly0bY5pcWKrdIOgdIhwe3Cqb4L5cIF1cW:wIH;mJJRp\SCmaYP0ZYwhSUuWLYDheIh4[XliYnnvcYFzc2W{czDpcoNtfWSrbnegVHJCWzRyLDDlTWY1TSxiNFWtRnAyNCCvVF;SMEBidmRiUEewJHM3KGurbnHz[UBqdiCjIITpcYUu\GWyZX7k[Y51KG2jbn7ldi=> MYGyN|k3PjZ{MR?=
C4-2  M4Toc2Z2dmO2aX;uJGF{e2G7 NIHuTmY2KM7:TR?= MXuwMVI1KGh? M2DJdYlvcGmkaYTzJJBpd3OyaH;yfYxifGmxbjDv[kB1cGViZHnzeIFtKEGNVD3wZZRpf2G7IHLpc41iemuncoOgbY5kdHWmaX7nJHBTSVN2MDyg[WlHPEVuIETFMWJROSxibWTPVkwh[W6mIGC3NEBUPiCtaX7hd4UhcW5iYTD0bY1mNWSncHXu[IVvfCCvYX7u[ZI> NVS3TZZqOjN7Nk[2NlE>
LNCaP NWTaNZJtT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHu1XGMyNTFyMECwJI5O M{LRblAuOyCm M{XkUYlvcGmkaYTzJINmdGxidnnhZoltcXS7IHTvd4Uh\GWyZX7k[Y51dHl? NYXOfop1OjN7Nk[2NlE>
C4-2  Mk\YS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1PNVFEuOTByMECgcm0> MnvjNE0{KGR? Ml6xbY5pcWKrdIOgZ4VtdCC4aXHibYxqfHliZH;z[UBl\XCnbnTlcpRtgQ>? NFTZdJozOzl4Nk[yNS=>
LNCaP NHfaOmtIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXuxNFAuPTByMDDuUS=> MXO3NkBp MXnpcoNz\WG|ZYOgeIhmKG[{YXP0bY9vKG:oIHPlcIx{KHWwZHXy[49qdmdiY3XscEBl\WG2aB?= NIfaWHYzOzl4Nk[yNS=>
C4-2  NX3UT3dxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NV\yeWNsOTByLUWwNFAhdk1? MW[3NkBp NXmxW5FGcW6lcnXhd4V{KHSqZTDmdoFkfGmxbjDv[kBk\WyuczD1coRmemexaX7nJINmdGxiZHXheIg> NGLvVWozOzl4Nk[yNS=>
PC-3 NIrrbWxHfW6ldHnvckBCe3OjeR?= MX:wMlUwOS9zMDFOwG0> MmHoOFghcA>? NHTKZY1ld3ewcnXneYxifGW|IITo[UBxcG:|cHjvdplt[XSrb36gc4Yh\G:5boP0doVidSCyYYToe4F6KHC{b4TlbY5{KGmwIHGg[I9{\S2mZYDlcoRmdnRibXHucoVz NInnOJEzOzJ3OEe0NC=>
DU145  NIXmU29HfW6ldHnvckBCe3OjeR?= NX;EVIlbOC53L{GvNVAh|ryP MU[0PEBp Mmjm[I94dnKnZ4XsZZRmeyC2aHWgdIhwe3Cqb4L5cIF1cW:wIH;mJIRwf26|dILlZY0heGG2aIfhfUBxem:2ZXnud{BqdiCjIHTvd4Uu\GWyZX7k[Y51KG2jbn7ldi=> NWr1WpBiOjN{NUi3OFA>
LNCaP NYK1dVdTS2WubDDWbYFjcWyrdImgRZN{[Xl? NF74RWgxNTFyMECgcm0> MYiwMVQh\A>? NV7Bd5hPemWmdXPl[EBNVkOjUDDj[YxtKH[rYXLpcIl1gSCrbjDhJIRwe2VvIHHu[EB1cW2nLXTldIVv\GWwdDDtZY5v\XMEoB?= MXiyN|I2QDd2MB?=
PC-3  NF3sfmVHfW6ldHnvckBCe3OjeR?= NHvZZlYyOCEQvF2= NWrrPVNFOTJiaB?= NXfQZ3A{cW6mdXPld{BifXSxcHjh[5k> M3y0N|I{OjV6N{Sw

... Click to View More Cell Line Experimental Data
Assay
Methods Test Index PMID
Western blot
pAKT / AKT / pGSK3β / GSK3β; 

PubMed: 26998062     


AZD5363 inhibited the phosphorylation of GSK3β, but increased the phosphorylation of AKT in a time-dependent manner in the (A) Hep-G2 cells. 

HER3 / pHER3 / HER2 / pHER2 / pPRAS40 / pS6 / p-4EBP1 / pFOXO / pERK / PARP / Cleaved PARP; 

PubMed: 26095475     


(A) BT474c or HCC1954 cells were treated for 24 h with increasing concentrations of AZD5363 ±0.3 μM or 1 μM AZD8931, respectively. Protein lysates were analysed by immunoblot with the indicated antibodies. Blots are representative of blots from 2–3 separate experiments. 

26998062 26095475
Immunofluorescence
p-Chk2 / γ-H2AX; 

PubMed: 29879757     


(C) Cells were treated with AZD1208 and AZD5363 alone or in combination for 5 days, and immunofluorescence analysis was subsequently performed. Confocal microscopy was used to observe the signals corresponding to p-Chk2 (red) and γ-H2AX (green). DAPI (blue) was used as a nuclear counterstain. CI, combination index. Scale bars=5 μm.

29879757
Growth inhibition assay
Cell viability; 

PubMed: 29879757     


Cells were seeded and cultured with increasing concentrations of AZD5363 and 1 μM AZD1208 every 3 days. The cells were cultured for 14 days until colonies formed and were then stained. The percentages of surviving cells were calculated by counting the number of colonies and are presented in a bar graph with standard error bars (n=3). a)p < 0.005. 

29879757
In vivo Oral dosing of AZD5363 (100, 300 mg/kg) to nude mice causes dose- and time-dependent reduction of PRAS40, GSK3β, and S6 phosphorylation in BT474c xenografts, reversible increases in blood glucose concentrations, and dose-dependent decreases in 2[18F]fluoro-2-deoxy-d-glucose (18F-FDG) uptake in U87-MG xenografts. Chronic oral dosing of AZD5363 (130, 200, and 300 mg/kg) causes dose-dependent growth inhibition of xenografts derived from various tumor types, including HER2+ breast cancer models that are resistant to trastuzumab. AZD5363 also significantly enhances the antitumor activity of docetaxel, lapatinib, and trastuzumab in breast cancer xenografts. [2]

Protocol

Kinase Assay:[1]
+ Expand

Caliper Off-Chip Incubation Mobility Shift assay:

The ability of AZD5363 and other compounds to inhibit the activity of AKT1, AKT2, and AKT3 is evaluated by the Caliper Off-Chip Incubation Mobility Shift assay. Active recombinant AKT1, AKT2, or AKT3 are incubated with a 5-FAM-labeled custom-synthesized peptide substrate together with increasing concentrations of inhibitor. Final reactions contained 1 to 3 nM AKT1, AKT2, or AKT3 enzymes; 1.5 mM peptide substrate; ATP at K m for each AKT isoform; 10 mM MgCl2, 4 mM DTT, 100 mM HEPES, and 0.015% Brij-35. The reactions are incubated at room temperature for 1 hour and stopped by the addition of buffer containing 100 mM HEPES, 0.015% Brij-35 solution, 0.1% coating reagent, 40 mM EDTA, and 5% DMSO. Plates are then analyzed using a Caliper LC3000, allowing for separation of peptide substrate and phosphorylated product by electrophoresis with subsequent detection and quantification of laser induced fluorescence.
Cell Research: [2]
+ Expand
  • Cell lines: 182 solid and hematologic tumor cell lines
  • Concentrations: ~30 μM
  • Incubation Time: 72 hours
  • Method: Cell proliferation assay is determined by 2 methods, MTS and Sytox Green. Briefly, cells are seeded in 96-well plates and incubated overnight at 37 ℃, 5% CO2. Cells are then exposed to concentrations of AZD5363 ranging from 30 to 0.003μM for 72 hours. For the MTS endpoint, cell proliferation is measured by the CellTiter AQueous Non-Radioactive Cell Proliferation Assay reagent in accordance with the manufacturer's protocol. For the Sytox Green endpoint, Sytox Green nucleic acid dye diluted in TBS-EDTA buffer is added to cells (final concentration of 0.13 μM) and the number of dead cells detected using an Acumen Explorer. Cells are then permeabilized by the addition of saponin (0.03% final concentration, diluted in TBS-EDTA buffer), incubated overnight and a total cell count measured. Predose measurements are made for both MTS and Sytox Green endpoints, and concentration needed to reduce the growth of treated cells to half that of untreated cells values are determined using absorbance readings (MTS) or live cell counts.
    (Only for Reference)
Animal Research:[2]
+ Expand
  • Animal Models: Female nude mice and male SCID mice with BT474c, U87MG, KPL-4, HCC-1187 xenografts.
  • Formulation: In 10% DMSO 25% w/v Kleptose HPB
  • Dosages: 130 mg/Kg - 300 mg/Kg
  • Administration: p.o.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 86 mg/mL (200.5 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
1% CMC Na
For best results, use promptly after mixing. 		30mg/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 428.92
Formula

C21H25ClN6O2
CAS No. 1143532-39-1
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03772561 Recruiting Solid Tumor Adult National University Hospital Singapore December 3 2018 Phase 1
NCT03772561 Recruiting Solid Tumor Adult National University Hospital Singapore December 3 2018 Phase 1
NCT03310541 Recruiting Breast Cancer|Prostate Cancer|Advanced Solid Tumors Memorial Sloan Kettering Cancer Center October 11 2017 Phase 1
NCT03310541 Recruiting Breast Cancer|Prostate Cancer|Advanced Solid Tumors Memorial Sloan Kettering Cancer Center October 11 2017 Phase 1
NCT03182634 Recruiting Advanced Breast Cancer Institute of Cancer Research United Kingdom|Royal Marsden NHS Foundation Trust December 15 2016 Phase 2
NCT03182634 Recruiting Advanced Breast Cancer Institute of Cancer Research United Kingdom|Royal Marsden NHS Foundation Trust December 15 2016 Phase 2

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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Akt Signaling Pathway Map

Akt Inhibitors with Unique Features

  • Selective Akt Inhibitor

    CCT128930 : Akt2-selective, IC50=6 nM.

  • Most Potent Akt Inhibitor

    GSK690693 : Akt1, IC50=2 nM; Akt2, IC50=13 nM; Akt3, IC50=9 nM.

  • Akt Inhibitor in Clinical Trial

    Perifosine (KRX-0401) : Phase III for relapsed and refractory multiple myeloma.

  • Classic Akt Inhibitor

    MK-2206 2HCl : Highly selective inhibitor of Akt1/2/3 with IC50 of 8 nM/12 nM/65 nM, respectively; no inhibitory activities against 250 other protein kinases observed. Phase 2.

Related Akt Products4

  • Afuresertib (GSK2110183) New

    Afuresertib (GSK2110183) is a potent, orally bioavailable Akt inhibitor with Ki of 0.08 nM, 2 nM, and 2.6 nM for Akt1, Akt2, and Akt3, respectively. Phase 2.

  • AT13148 New

    AT13148 is an oral, ATP-competitive, multi-AGC kinase inhibitor with IC50 of 38 nM/402 nM/50 nM, 8 nM, 3 nM, and 6 nM/4 nM for Akt1/2/3, p70S6K, PKA, and ROCKI/II, respectively. Phase 1.

  • SC79 New

    SC79 is a brain-penetrable Akt phosphorylation activator and an inhibitor of Akt-PH domain translocation.

  • MK-2206 2HCl

    MK-2206 2HCl is a highly selective inhibitor of Akt1/2/3 with IC50 of 8 nM/12 nM/65 nM in cell-free assays, respectively; no inhibitory activities against 250 other protein kinases observed. Phase 2.

    Features:The first allosteric small molecule inhibitor of Akt to enter clinical development.

  • Ipatasertib (GDC-0068)

    Ipatasertib (GDC-0068) is a highly selective pan-Akt inhibitor targeting Akt1/2/3 with IC50 of 5 nM/18 nM/8 nM in cell-free assays, 620-fold selectivity over PKA. Phase 2.

  • GSK690693

    GSK690693 is a pan-Akt inhibitor targeting Akt1/2/3 with IC50 of 2 nM/13 nM/9 nM in cell-free assays, also sensitive to the AGC kinase family: PKA, PrkX and PKC isozymes. Phase 1.

  • Perifosine (KRX-0401)

    Perifosine (KRX-0401) is a novel Akt inhibitor with IC50 of 4.7 μM in MM.1S cells, targets pleckstrin homology domain of Akt. Phase 3.

  • A-674563

    A-674563 is an Akt1 inhibitor with Ki of 11 nM in cell-free assays, modest potent to PKA and >30-fold selective for Akt1 over PKC.

    Features:Orally bioavailable compound (achieved by replacing indole of A-443654 with phenyl moiety) and somewhat less selective for Akt over PKA than A-443654.

  • Triciribine

    Triciribine is a DNA synthesis inhibitor, also inhibits Akt in PC3 cell line and HIV-1 in CEM-SS, H9, H9IIIB, U1 cells with IC50 of 130 nM and 20 nM, respectively; does not inhibit PI3K/PDK1; 5000-fold less active in cells lacking adenosine kinase. Phase 1/2.

  • Honokiol

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

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID