Catalog No.S7009

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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Cited by 4 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 MWHDfZRwfG:6aXRCpIF{e2G7 MoH1N{4{KM7:TR?= M1LubVMh\GG7cx?= MUHQc5RmdnSrYYTpc44hd2ZiY3;uZZR2dXWvYXKtbY5lfWOnZDDjfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDMU3gh[2WubIOgZZQhOy5|IIXNJIFnfGW{IEOg[IF6eyCkeTDNWHMh[XO|YYm= NWDUbXpGOjRyOEO3PFI>
human BxPC3 cells M3rZUGN6fG:2b4jpZ:Kh[XO|YYm= M2fzWFMvOyEQvF2= M3uwdVUh\GG7cx?= MU\Qc5RmdnSrYYTpc44hd2ZiY3;uZZR2dXWvYXKtbY5lfWOnZDDjfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDCfHBEOyClZXzsd{BifCB|LkOgeW0h[W[2ZYKgOUBl[Xm|IHL5JG1VWyCjc4PhfS=> M3XxOlI1ODh|N{iy
human LS180 cells NYH1[GZpS3m2b4TvfIlkyqCjc4PhfS=> M4HPUlMvOyEQvF2= MW[1JIRigXN? NFezOmxRd3SnboTpZZRqd25ib3[gZ49v[XS3bYXtZYIucW6mdXPl[EBkgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBNWzF6MDDj[YxteyCjdDCzMlMhfU1iYX\0[ZIhPSCmYYnzJIJ6KE2WUzDhd5NigQ>? MmXuNlQxQDN5OEK=
human HCT15 cells NWLLV21zS3m2b4TvfIlkyqCjc4PhfS=> MVKzMlMh|ryP NV3zOYV4PSCmYYnz M2HnOnBwfGWwdHnheIlwdiCxZjDjc45ifHWvdX3hZk1qdmS3Y3XkJIN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGhEXDF3IHPlcIx{KGG2IEOuN{B2VSCjZoTldkA2KGSjeYOgZpkhVVSVIHHzd4F6 NGH5fWozPDB6M{e4Ni=>
human H460 cells Mnz6R5l1d3SxeHnjxsBie3OjeR?= NIHiPFc{NjNizszN MXq1JIRigXN? NHX4PHBRd3SnboTpZZRqd25ib3[gZ49v[XS3bYXtZYIucW6mdXPl[EBkgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBJPDZyIHPlcIx{KGG2IEOuN{B2VSCjZoTldkA2KGSjeYOgZpkhVVSVIHHzd4F6 Mmm0NlQxQDN5OEK=
human SW620 cells NX\oTpJ4S3m2b4TvfIlkyqCjc4PhfS=> NXzPNZFQOy5|IN88US=> MomwOUBl[Xm| NEDleJZRd3SnboTpZZRqd25ib3[gZ49v[XS3bYXtZYIucW6mdXPl[EBkgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBUXzZ{MDDj[YxteyCjdDCzMlMhfU1iYX\0[ZIhPSCmYYnzJIJ6KE2WUzDhd5NigQ>? MVmyOFA5Ozd6Mh?=
human SW620 cells M2LMWmN6fG:2b4jpZ:Kh[XO|YYm= MnX6NU4yKM7:TR?= MmjZOUBl[Xm| MlnQVI91\W62aXH0bY9vKG:oIHPvcoF1fW23bXHiMYlv\HWlZXSgZ5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gV3c3OjBiY3XscJMh[XRiMT6xJJVOKGGodHXyJFUh\GG7czDifUBOXFNiYYPzZZk> MkXhNlQxQDN5OEK=
human Capan1 cells MmDRR5l1d3SxeHnjxsBie3OjeR?= MorYNk42KM7:TR?= NWfaPXNFPSCmYYnz MYnQc5RmdnSrYYTpc44hd2ZiY3;uZZR2dXWvYXKtbY5lfWOnZDDhdI9xfG:|aYOgbY4hcHWvYX6gR4Fx[W5zIHPlcIx{KGG2IEKuOUB2VSCjZoTldkA2KGSjeYOgZpkhVVSVIHHzd4F6 MlLONlQxQTN7NEC=
human SKMES1 cells MkH6R5l1d3SxeHnjxsBie3OjeR?= MUSyMlUh|ryP Mlf1OUBl[Xm| MliwVI91\W62aXH0bY9vKG:oIHPvcoF1fW23bXHiMYlv\HWlZXSgZZBweHSxc3nzJIlvKGi3bXHuJHNMVUWVMTDj[YxteyCjdDCyMlUhfU1iYX\0[ZIhPSCmYYnzJIJ6KE2WUzDhd5NigQ>? MkC0NlQxQTN7NEC=
human PC3 cells MXnBdI9xfG:|aYOgZZN{[Xl? MoLwNk42KM7:TR?= NG\HcVc2KGSjeYO= MVHJcoR2[3Srb36gc4Yhe2Wwc3n0bZpifGmxbjDv[kBpfW2jbjDQR|Mh[2WubIOgeI8h[2:wYYT1cZVu[WJvaX7keYNm\CCjcH;weI9{cXNiYYPz[ZN{\WRiYYOgZ4VtdCC4aXHibYxqfHliYYSgNk42KHWPIHHmeIVzKDViZHH5d{BjgSCPVGOgZZN{[Xl? NUj0Uld[OjRyOUO5OFA>
human AGS cells MULBdI9xfG:|aYOgZZN{[Xl? NXu4U|ZvOi53IN88US=> NXfoT3puPSCmYYnz MkHlTY5lfWO2aX;uJI9nKHOnboPpeIl7[XSrb36gc4YhcHWvYX6gRWdUKGOnbHzzJJRwKGOxbnH0eY12dWGkLXnu[JVk\WRiYYDvdJRwe2m|IHHzd4V{e2WmIHHzJINmdGxidnnhZoltcXS7IHH0JFIvPSC3TTDh[pRmeiB3IHThfZMh[nliTWTTJIF{e2G7 M1XH[FI1ODl|OUSw
human U118MG cells NFvQelVCeG:ydH;zbZMh[XO|YYm= NGrqTIwzNjVizszN M2i4eFUh\GG7cx?= M3W3cHBwfGWwdHnheIlwdiCxZjDjc45ifHWvdX3hZk1qdmS3Y3XkJIFxd3C2b4Ppd{BqdiCqdX3hckBWOTF6TVegZ4VtdHNiYYSgNk42KHWPIHHmeIVzKDViZHH5d{BjgSCPVGOgZZN{[Xl? NYLVcVM{OjRyOUO5OFA>
human SKMES1 cells NWfxVZhnSXCxcITvd4l{KGG|c3H5 NIWwNGozNjVizszN NFvXcXE2KGSjeYO= MWrQc5RmdnSrYYTpc44hd2ZiY3;uZZR2dXWvYXKtbY5lfWOnZDDhdI9xfG:|aYOgbY4hcHWvYX6gV2tOTVNzIHPlcIx{KGG2IEKuOUB2VSCjZoTldkA2KGSjeYOgZpkhVVSVIHHzd4F6yqB? MYSyOFA6Ozl2MB?=
human Capan1 cells NXnDV5Q6SXCxcITvd4l{KGG|c3H5 MnX4Nk42KM7:TR?= NYDEdYJ{PSCmYYnz NHHoW|JRd3SnboTpZZRqd25ib3[gZ49v[XS3bYXtZYIucW6mdXPl[EBieG:ydH;zbZMhcW5iaIXtZY4hS2GyYX6xJINmdGy|IHH0JFIvPSC3TTDh[pRmeiB3IHThfZMh[nliTWTTJIF{e2G7 NFPMdYQzPDB7M{m0NC=>
human MDA-MB-231 cells M4TvZmZ2dmO2aX;uJIF{e2G7 NFfPS4QxNjN5LUOuN{DPxE1? M2X2cVE6KGh? NHn0WWpKdmirYnn0bY9vKG:oIHPJRXAyNzJiaX6gbJVu[W5iTVTBMW1DNTJ|MTDj[YxteyCjc4Pld5Nm\CCjczDpcoR2[3Srb36gc4YhXE6IYXzwbIEhdGW4ZXygZZQhOC5|NzD0c{A{NjNidV2gZYZ1\XJiMUmgbJJ{KGK7IFXMTXNCyqB? NGLDd5UzPDB7M{m0NC=>

... Click to View More Cell Line Experimental Data

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:


+ Expand
  • 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

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT03111992 Recruiting 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