For research use only.

Catalog No.S7009

14 publications

LCL161 Chemical Structure

Molecular Weight(MW): 500.63

LCL-161, a small molecule second mitochondrial activator of caspase (SMAC) mimetic, potently binds to and inhibits multiple IAPs (i.e. XIAP, c-IAP).

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Selleck's LCL161 has been cited by 14 publications

2 Customer Reviews

  • Parental or rVCR RD cells were either left untreated (UT) or exposed to 40 μM of LCL161 in the absence or presence of PSC-833 (10 μM) for 48 h before analysis of DNA fragmentation using PI staining and flow cytometry (data shown are mean + SD, n = 3). *, p < 0.05, **, p < 0.01, ***, p < 0.001.

    Cancer Lett, 2018, 440-441:126-134. LCL161 purchased from Selleck.

  • The Smac mimetic LCL-161, which inhibits cIAP1, modestly sensitizes hair cells to gentamicin damage. (A) Variable LCL-161 concentrations do not affect toxicity to 50 μM neomycin (one-way ANOVA, F4,69 = 1.54, p = 0.199). (B) Variable LCL has a modest but significant effect on gentamicin toxicity (one-way ANOVA, F4,31 = 3.14, p = 0.028), with 10 μM LCL conveying significant sensitization (∗p < 0.05).

    Front Cell Neurosci, 2017, LCL161 purchased from Selleck.

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Biological Activity

Description LCL-161, a small molecule second mitochondrial activator of caspase (SMAC) mimetic, potently binds to and inhibits multiple IAPs (i.e. XIAP, c-IAP).
cIAP [1] XIAP [1]
In vitro

LCL161 binds to inhibitors of apoptosis proteins (IAPs) with high affinity and initiates the destruction of cIAP1 and cIAP2, which further induces apoptosis via caspase activation. LCL161 modestly inhibits the growth of FLT3-ITD-expressing cells when administered alone, with an IC50 ranging from ~0.5 μM (Ba/F3-FLT3-ITD cells) to ~4 μM (MOLM13-luc+ cells). The potency of LCL161 against the D835Y mutant is observed to be considerably higher, with an IC50 of ~50 nM when tested against Ba/F3-D835Y cells. Treatment of MOLM13-luc+ cells with a combination of LCL161 and PKC412 leads to significantly more killing of cells than either agent alone, with Calcusyn combination indices suggestive of synergy. PKC412 and LCL161 induces apoptosis of MOLM13-luc+ cells. The combination of PKC412 and LCL161 leads to a higher induction of apoptosis than either agent alone. LCL161 is able to override stromal-mediated rescue of mutant FLT3-expressing cells through positive combination with PKC412. LCL161 inhibits the growth of Ba/F3.p210 cells with an IC50 of ~100 nM. The combination of LCL161 and the ABL inhibitor, imatinib, is observed to be synergistic against BCR-ABL-expressing cells. LCL161 also has demonstrated activity against drug-resistant cells expressing point mutations in the target proteins. LCL161 at 1000 nM is able to mostly or completely kill Ba/F3-derived cell lines conferring resistance to PKC412, which express FLT3-ITD harboring point mutations in the ATP-binding pocket of FLT3. LCL161 also shows activity at concentrations ranging from 100 to 1000 nM against Ba/F3 cells expressing various imatinib- and nilotinib-resistant BCR-ABL point mutations. [1] LCL161 is evaluated against the 23 cell lines in the Pediatric Preclinical Testing Program (PPTP) in vitro panel using 96 hr. LCL161 achieves 50% growth inhibition against only 3 of the 23 tested PPTP cell lines under concentration of 10 μM. The three cell lines includes two T-cell ALL cell lines (COG-LL-317 and CCRF-CEM) and an anaplastic large cell lymphoma cell line (Karpas-299), with CCRF-CEM and Karpas-299 showing the lowest relative IC50 values (0.25 and 1.6 μM, respectively). [2] LCL161shows immunomodulatory properties on human immune subsets. T lymphocytes treated with LCL161 demonstrates significantly enhanced cytokine secretion upon activation, with little effect on CD4 and CD8 T-cell survival or proliferation. LCL161 treatment of peripheral blood mononuclear cells significantly enhances priming of naïve T cells with synthetic peptides in vitro. Myeloid dendritic cells undergoes phenotypic maturation upon LCL161 and demonstrates a reduced capacity to cross-present a tumor antigen-based vaccine. These effects are potentially mediated through an observed activation of the canonical and non-canonical NF-κB pathways, following LCL161 with a resulting upregulation of anti-apoptotic molecules. [3]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human LOX cells M4L6dGN6fG:2b4jpZ:Kh[XO|YYm= MnLLN{4{KM7:TR?= NY\odVB3OyCmYYnz NX\TemRTWG:2ZX70bYF1cW:wIH;mJINwdmG2dX31cYFjNWmwZIXj[YQh[3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hVE:[IHPlcIx{KGG2IEOuN{B2VSCjZoTldkA{KGSjeYOgZpkhVVSVIHHzd4F6 NEHIUGczPDB6M{e4Ni=>
human BxPC3 cells NF36b|lEgXSxdH;4bYPDqGG|c3H5 NYjCfW9QOy5|IN88US=> MXW1JIRigXN? M2HtdHBwfGWwdHnheIlwdiCxZjDjc45ifHWvdX3hZk1qdmS3Y3XkJIN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGJ5WEN|IHPlcIx{KGG2IEOuN{B2VSCjZoTldkA2KGSjeYOgZpkhVVSVIHHzd4F6 NYjsdlRrOjRyOEO3PFI>
human LS180 cells MV7DfZRwfG:6aXRCpIF{e2G7 MXmzMlMh|ryP Mlv6OUBl[Xm| MW\Qc5RmdnSrYYTpc44hd2ZiY3;uZZR2dXWvYXKtbY5lfWOnZDDjfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDMV|E5OCClZXzsd{BifCB|LkOgeW0h[W[2ZYKgOUBl[Xm|IHL5JG1VWyCjc4PhfS=> MV2yOFA5Ozd6Mh?=
human HCT15 cells NFzIZpFEgXSxdH;4bYPDqGG|c3H5 M2LIXlMvOyEQvF2= MlTwOUBl[Xm| NH;VT3ZRd3SnboTpZZRqd25ib3[gZ49v[XS3bYXtZYIucW6mdXPl[EBkgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBJS1RzNTDj[YxteyCjdDCzMlMhfU1iYX\0[ZIhPSCmYYnzJIJ6KE2WUzDhd5NigQ>? M37SOVI1ODh|N{iy
human H460 cells NXjieVdHS3m2b4TvfIlkyqCjc4PhfS=> MmWxN{4{KM7:TR?= MVS1JIRigXN? M1G1cnBwfGWwdHnheIlwdiCxZjDjc45ifHWvdX3hZk1qdmS3Y3XkJIN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGg1PjBiY3XscJMh[XRiMz6zJJVOKGGodHXyJFUh\GG7czDifUBOXFNiYYPzZZk> NF;pbXczPDB6M{e4Ni=>
human SW620 cells NEK4N4hEgXSxdH;4bYPDqGG|c3H5 NYTMVIZGOy5|IN88US=> MWW1JIRigXN? NWPHTlBHWG:2ZX70bYF1cW:wIH;mJINwdmG2dX31cYFjNWmwZIXj[YQh[3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hW1d4MkCgZ4VtdHNiYYSgN{4{KHWPIHHmeIVzKDViZHH5d{BjgSCPVGOgZZN{[Xl? M1vyR|I1ODh|N{iy
human SW620 cells NGrrcHVEgXSxdH;4bYPDqGG|c3H5 NX;5[YJpOS5zIN88US=> M4DOdFUh\GG7cx?= NHLGS3lRd3SnboTpZZRqd25ib3[gZ49v[XS3bYXtZYIucW6mdXPl[EBkgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBUXzZ{MDDj[YxteyCjdDCxMlEhfU1iYX\0[ZIhPSCmYYnzJIJ6KE2WUzDhd5NigQ>? MUGyOFA5Ozd6Mh?=
human Capan1 cells MlPnR5l1d3SxeHnjxsBie3OjeR?= MVKyMlUh|ryP MVe1JIRigXN? M1TzTHBwfGWwdHnheIlwdiCxZjDjc45ifHWvdX3hZk1qdmS3Y3XkJIFxd3C2b4Ppd{BqdiCqdX3hckBE[XCjbkGgZ4VtdHNiYYSgNk42KHWPIHHmeIVzKDViZHH5d{BjgSCPVGOgZZN{[Xl? NXfPV|d3OjRyOUO5OFA>
human SKMES1 cells Mk\hR5l1d3SxeHnjxsBie3OjeR?= NHPpVoszNjVizszN NGDNRXU2KGSjeYO= MX\Qc5RmdnSrYYTpc44hd2ZiY3;uZZR2dXWvYXKtbY5lfWOnZDDhdI9xfG:|aYOgbY4hcHWvYX6gV2tOTVNzIHPlcIx{KGG2IEKuOUB2VSCjZoTldkA2KGSjeYOgZpkhVVSVIHHzd4F6 MUWyOFA6Ozl2MB?=
human PC3 cells NXnY[GtOSXCxcITvd4l{KGG|c3H5 MVKyMlUh|ryP M2PoU|Uh\GG7cx?= MlHwTY5lfWO2aX;uJI9nKHOnboPpeIl7[XSrb36gc4YhcHWvYX6gVGM{KGOnbHzzJJRwKGOxbnH0eY12dWGkLXnu[JVk\WRiYYDvdJRwe2m|IHHzd4V{e2WmIHHzJINmdGxidnnhZoltcXS7IHH0JFIvPSC3TTDh[pRmeiB3IHThfZMh[nliTWTTJIF{e2G7 MnHZNlQxQTN7NEC=
human AGS cells NUP2TZUzSXCxcITvd4l{KGG|c3H5 MUWyMlUh|ryP MnTwOUBl[Xm| NVPUUINVUW6mdXP0bY9vKG:oIIPlcpNqfGm8YYTpc44hd2ZiaIXtZY4hSUeVIHPlcIx{KHSxIHPvcoF1fW23bXHiMYlv\HWlZXSgZZBweHSxc3nzJIF{e2W|c3XkJIF{KGOnbHygeoli[mmuaYT5JIF1KDJwNTD1UUBi\nSncjC1JIRigXNiYomgUXRUKGG|c3H5 NIXESlAzPDB7M{m0NC=>
human U118MG cells MkfrRZBweHSxc3nzJIF{e2G7 M1HFPVIvPSEQvF2= NY[5ZlE1PSCmYYnz NVXrfYtvWG:2ZX70bYF1cW:wIH;mJINwdmG2dX31cYFjNWmwZIXj[YQh[XCxcITvd4l{KGmwIHj1cYFvKFVzMUjNS{Bk\WyuczDheEAzNjVidV2gZYZ1\XJiNTDkZZl{KGK7IF3UV{Bie3OjeR?= NX32R4M6OjRyOUO5OFA>
human SKMES1 cells MV3BdI9xfG:|aYOgZZN{[Xl? NETYfIwzNjVizszN Mnm3OUBl[Xm| NXPFXmdzWG:2ZX70bYF1cW:wIH;mJINwdmG2dX31cYFjNWmwZIXj[YQh[XCxcITvd4l{KGmwIHj1cYFvKFONTVXTNUBk\WyuczDheEAzNjVidV2gZYZ1\XJiNTDkZZl{KGK7IF3UV{Bie3OjedMg NYX2V2t2OjRyOUO5OFA>
human Capan1 cells MmDYRZBweHSxc3nzJIF{e2G7 NEfYWogzNjVizszN NF7UfWY2KGSjeYO= NVKyfol7WG:2ZX70bYF1cW:wIH;mJINwdmG2dX31cYFjNWmwZIXj[YQh[XCxcITvd4l{KGmwIHj1cYFvKEOjcHHuNUBk\WyuczDheEAzNjVidV2gZYZ1\XJiNTDkZZl{KGK7IF3UV{Bie3OjeR?= MYmyOFA6Ozl2MB?=
human MDA-MB-231 cells M4qwUWZ2dmO2aX;uJIF{e2G7 MVuwMlM4NTNwMzFOwG0> NHThdpQyQSCq MkXMTY5pcWKrdHnvckBw\iClSVHQNU8zKGmwIHj1cYFvKE2GQT3NRk0zOzFiY3XscJMh[XO|ZYPz[YQh[XNiaX7keYN1cW:wIH;mJHRPTmGucHjhJIxmfmWuIHH0JFAvOzdidH:gN{4{KHWPIHHmeIVzKDF7IHjyd{BjgSCHTFnTReKh M3XT[lI1ODl|OUSw

... Click to View More Cell Line Experimental Data

Methods Test Index PMID
Western blot
cIAP1 / cIAP2 / XIAP / surivivin ; 

PubMed: 27737687     

A549 and H460 cells were treated for 48 h with 0-20 μM LCL161. The protein levels of cIAP1, cIAP2, XIAP and survivin were assessed by western blotting. β-actin was used as a loading control. The bar graphs represent the mean ± SD of different proteins/β-actin; *P < 0.05; **P < 0.01; ***P < 0.001

Growth inhibition assay
Cell viability; 

PubMed: 27737687     

Cells were treated for 48 h with the indicated concentrations of LCL161 and paclitaxel (c) or for the indicated times with 10 μM LCL161 and/or 10 μM paclitaxel (d). Cell viability was determined by the MTT assay. Data are represented as mean ± SD; *P < 0.05; **P < 0.01; ***P < 0.001

In vivo LCL161 significantly enhances the ability of PKC412 to inhibit the growth of Ba/F3-FLT3-ITD-luc+ cells in vivo. LCL161 is also shown to positively combine with the standard chemotherapeutic agents, Ara-c and doxorubicin, against FLT3-ITD-expressing cells and against D835Y-expressing cells. There is an additive effect achieved by combining both Nilotinib and LCL161 in suppressing leukemia growth. LCL161 (100 mg/kg) enhances in vivo effects of high-moderate doses of nilotinib (100 mg/kg) on leukemia burden in mice. [1] CL161 is tested against the Pediatric Preclinical Testing Program (PPTP) in vivo panels (30 or 75 mg/kg [solid tumors] or 100 mg/kg [ALL]) administered orally twice in a week. LCL161 induces significant differences in EFS distribution in approximately one-third of solid tumor xenografts (osteosarcoma and glioblastoma), but not in ALL xenografts. No objective tumor responses are observed. In vivo LCL161 demonstrates limited single agent activity against the pediatric preclinical models studied. [2]


Cell Research:


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  • Cell lines: Human T-cell ALL cell lines COG-LL-317
  • Concentrations: ~10 μM
  • Incubation Time: 96 hours
  • Method:

    In vitro testing is performed using DIMSCAN

    (Only for Reference)

Solubility (25°C)

In vitro DMSO 100 mg/mL (199.74 mM)
Ethanol 20 mg/mL warmed (39.94 mM)
Water Insoluble

* 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 500.63


CAS No. 1005342-46-0
Storage powder
in solvent
Synonyms N/A
Smiles CC(C(=O)NC(C1CCCCC1)C(=O)N2CCCC2C3=NC(=CS3)C(=O)C4=CC=C(C=C4)F)NC

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT03111992 Completed Drug: PDR001|Drug: CJM112|Drug: LCL161 Multiple Myeloma Novartis Pharmaceuticals|Novartis December 18 2017 Phase 1
NCT01934634 Unknown status Drug: LCL161|Drug: Gemcitabine|Drug: nab-Paclitaxel Metastatic Pancreatic Cancer US Oncology Research|Novartis Pharmaceuticals|Delta Clinical Research LLC March 2014 Phase 1
NCT01968915 Completed Drug: LCL161|Drug: Paclitaxel Neoplasms Novartis Pharmaceuticals|Novartis November 2013 Phase 1
NCT01617668 Completed Drug: LCL161|Drug: paclitaxel Breast Cancer Novartis Pharmaceuticals|Novartis August 2012 Phase 2

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IAP Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID