APR-246 (PRIMA-1MET)

Catalog No.S7724

APR-246 (PRIMA-1MET) Chemical Structure

Molecular Weight(MW): 199.25

APR-246, also known as PRIMA-1MET, is a small organic molecule that has been shown to restore tumour-suppressor function primarily to mutant p53 and also to induce cell death in various cancer types.

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Biological Activity

Description APR-246, also known as PRIMA-1MET, is a small organic molecule that has been shown to restore tumour-suppressor function primarily to mutant p53 and also to induce cell death in various cancer types.
Targets
Mutant p53 [2]
()
In vitro

APR-246 (PRIMA-1MET) is the first clinical-stage compound that reactivates mutant p53 and induces apoptosis. APR-246 is a prodrug that is converted to the active compound methylene quinuclidinone (MQ), a Michael acceptor that binds to cysteine residues in mutant p53 and restores its wild-type conformation. APR-246 completely restores the cisplatin and doxorubicin sensitivity to p53-mutant drug-resistant ovarian cancer cells. It not only reactivates p53 but also decreases intracellular glutathione levels in a dose-dependent manner. APR-246 can trigger apoptosis in a p53-independent manner by inducing ROS and endoplasmic reticulum (ER) stress and by inhibiting thioredoxin reductase 1 (TrxR1). It was also reported that APR-246 induces cell death in myeloma cells independently of p53 status by impairing the GSH/ROS balance[1]. PRIMA-1Met/APR-246 efficiently inhibited the growth of the SCLC cell lines expressing mutant p53 in vitro and induced apoptosis, associated with increased fraction of cells with fragmented DNA, caspase-3 activation, PARP cleavage, Bax and Noxa upregulation and Bcl-2 downregulation in the cells[2].

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
NALM-6 M2fqT2NmdGxidnnhZoltcXS7IHHzd4F6 MnrEbIlocCC|ZX7zbZRqfmm2eTDhcoQh[2WubDDk[YF1cCCrbnT1Z5Rqd25iaX6gZYxtKFSSNUPteZQhdGW3a3XtbYF{NCCkdYSgcI94KEGSUj2yOFYhe2Wwc3n0bZZqfHliaX6gWHA2O3e2IFHMUC=> NHHyNVM{OTB5M{C3Oi=>
UoCB-6 NVi4WIpsS2WubDD2bYFjcWyrdImgZZN{[Xl? MW\obYdpKHOnboPpeIl3cXS7IHHu[EBk\WyuIHTlZZRpKGmwZIXjeIlwdiCrbjDhcIwhXFB3M331eEBt\XWtZX3pZZMtKGK3dDDsc5chSVCULUK0OkB{\W6|aYTpeol1gSCrbjDUVFU{f3RiQVzM NFvZeY8{OTB5M{C3Oi=>
EU-3 NX7v[mpLS2WubDD2bYFjcWyrdImgZZN{[Xl? NXLseJE1cGmpaDDz[Y5{cXSrdnn0fUBidmRiY3XscEBl\WG2aDDpcoR2[3Srb36gbY4h[WyuIGTQOVNufXRibHX1b4VucWG|LDDieZQhdG:5IFHQVk0zPDZic3Xud4l1cX[rdImgbY4hXFB3M4f0JGFNVA>? NITic3U{OTB5M{C3Oi=>
MUTZ-5 MX;D[YxtKH[rYXLpcIl1gSCjc4PhfS=> MmHCbIlocCC|ZX7zbZRqfmm2eTDhcoQh[2WubDDk[YF1cCCrbnT1Z5Rqd25iaX6gZYxtKFSSNUPteZQhdGW3a3XtbYF{NCCkdYSgcI94KEGSUj2yOFYhe2Wwc3n0bZZqfHliaX6gWHA2O3e2IFHMUC=> NIHhbpQ{OTB5M{C3Oi=>
KOPN-8 NUTudHdmS2WubDD2bYFjcWyrdImgZZN{[Xl? MX3obYdpKHOnboPpeIl3cXS7IHHu[EBk\WyuIHTlZZRpKGmwZIXjeIlwdiCrbjDhcIwhXFB3M331eEBt\XWtZX3pZZMtKGK3dDDsc5chSVCULUK0OkB{\W6|aYTpeol1gSCrbjDUVFU{f3RiQVzM NHr3T5g{OTB5M{C3Oi=>
RS4;11 NVO3boZpS2WubDD2bYFjcWyrdImgZZN{[Xl? NWT4eHhjcGmpaDDz[Y5{cXSrdnn0fUBidmRiY3XscEBl\WG2aDDpcoR2[3Srb36gbY4h[WyuIGTQOVNufXRibHX1b4VucWG|LDDieZQhdG:5IFHQVk0zPDZic3Xud4l1cX[rdImgbY4hXFB3M4f0JGFNVA>? MYezNVA4OzB5Nh?=
SKBR3 MUnD[YxtKGO7Y3zlJIF{e2G7 NGDsOFE2KML3TR?= NUX3T5ZDOiC5ZXXrdy=> MoT0cIFx[XSrbnniJIlvKGOxbXLpcoF1cW:wIIfpeIghSVCULUK0OkBk[XW|ZXSgZUBtd3encjDs[ZZmdCCxZjDHNUBienKnc4SgZY5lKGGwIHnuZ5Jm[XOnIHnuJJRp\SC|dXKtS|Eh\nKjY4Tpc44> M1L2flMxPzR|OUm2
BT549 NXr4cow3S2WubDD2bYFjcWyrdImgZZN{[Xl? M1TRWGlEPTB;Mz6xJO69VQ>? NWjWOm9FOzBzOU[yN|Y>
MDA-MB-468 M4D4O2NmdGxidnnhZoltcXS7IHHzd4F6 NHrEd|ZKSzVyPUWg{txO M1vYc|MxOTl4MkO2
MDA-MB-231 NGLzWINE\WyuII\pZYJqdGm2eTDhd5NigQ>? MYLJR|UxRTRwMTFOwG0> MYmzNFE6PjJ|Nh?=
HCC1143 NYHZfWRoS2WubDD2bYFjcWyrdImgZZN{[Xl? M{\lfGlEPTB;Nj64JO69VQ>? NGPxUHk{ODF7NkKzOi=>
MDA-MB-453 MXzD[YxtKH[rYXLpcIl1gSCjc4PhfS=> Moe3TWM2OD1yLkmg{txO MV:zNFE6PjJ|Nh?=
SKBR3 M2\lemNmdGxidnnhZoltcXS7IHHzd4F6 M{HZemlEPTB;NT6xJO69VQ>? MWSzNFE6PjJ|Nh?=
UACC812 MkjtR4VtdCC4aXHibYxqfHliYYPzZZk> M1Wyb2lEPTB;MUGuN{DPxE1? NX3uR4hwOzBzOU[yN|Y>
MCF7 NYTTZ49tS2WubDD2bYFjcWyrdImgZZN{[Xl? NFfzZnRKSzVyPUOxMlEh|ryP MVqzNFE6PjJ|Nh?=
MCF10A NIL5VW9E\WyuII\pZYJqdGm2eTDhd5NigQ>? NIK5XWVKSzVyPUWuNkDPxE1? NGPybZQ{ODF7NkKzOi=>
UMSCC10A NH3uNpZE\WyuII\pZYJqdGm2eTDhd5NigQ>? M3X6W|AuPTBizszN MWG3NkBp MX7zeZBxemW|c3XkJINmdGxic4Xyeol3[WxiYX7kJIJwemViYTDtc4Rme3RiZX\m[YN1KG:wIITo[UBscWyuaX7nJI9nKEiQU1PDJINmdGy| MkXFNlk{PDh2NkK=
FaDu M1ftU2NmdGxidnnhZoltcXS7IHHzd4F6 NIDsTXAxNTVyIN88US=> MVu3NkBp MoDrd5VxeHKnc4Pl[EBk\WyuIIP1dpZqfmGuIHHu[EBjd3KnIHGgcY9l\XO2IHXm[oVkfCCxbjD0bIUhc2mubHnu[{Bw\iCKTmPDR{Bk\Wyucx?= NHnhb4YzQTN2OES2Ni=>

... Click to View More Cell Line Experimental Data

In vivo APR-246 showed a good safety profile in a Phase I/II clinical dose-finding study on hematological malignancies and prostate cancer and both clinical and p53-dependent biological responses were observed. In animal studies, APR-246 is well tolerated. Single treatment with APR-246 inhibits tumor growth by 21% in mice bearing the aggressively growing A2780-CP20 tumor xenografts[1].

Protocol

Cell Research:

[1]

+ Expand
  • Cell lines: OVCAR-3 cells
  • Concentrations: 40 μM
  • Incubation Time: 20 h
  • Method:

    OVCAR-3 cells were plated at a density of 75 000 cells per well in 3 ml of medium in 12-well plates. Next day, 2.5 ml medium was removed and cells were treated with cisplatin or APR-246 or in combination for 20 h. Next day, cells were harvested by trypsinization, washed twice and cells were stained with Annexin V and propidium iodine (PI). After staining, the samples were analyzed by LSRII flow cytometer. 


    (Only for Reference)
Animal Research:

[1]

+ Expand
  • Animal Models: CD-1 Nu/Nu mice
  • Formulation: PBS
  • Dosages: 400 mg/kg/day
  • Administration: i.v.
    (Only for Reference)

Solubility (25°C)

Chemical Information

Molecular Weight 199.25
Formula

C10H17NO3

CAS No. 5291-32-7
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03745716 Recruiting MDS Aprea Therapeutics AB January 11 2019 Phase 3
NCT03745716 Recruiting MDS Aprea Therapeutics AB January 11 2019 Phase 3
NCT03588078 Recruiting Myelodysplastic Syndrome With Gene Mutation|Acute Myeloid Leukemia With Gene Mutations|Myeloproliferative Neoplasm|Chronic Myelomonocytic Leukemia Groupe Francophone des Myelodysplasies|Aprea Therapeutics AB September 15 2018 Phase 1|Phase 2
NCT03588078 Recruiting Myelodysplastic Syndrome With Gene Mutation|Acute Myeloid Leukemia With Gene Mutations|Myeloproliferative Neoplasm|Chronic Myelomonocytic Leukemia Groupe Francophone des Myelodysplasies|Aprea Therapeutics AB September 15 2018 Phase 1|Phase 2
NCT03391050 Active not recruiting Melanoma Aprea Therapeutics AB|Jules Bordet Institute January 18 2018 Phase 1|Phase 2
NCT03391050 Active not recruiting Melanoma Aprea Therapeutics AB|Jules Bordet Institute January 18 2018 Phase 1|Phase 2

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID