1. PI3K/Akt/mTOR
    Autophagy
  2. PI3K
    Autophagy

CAL-101 (Synonyms: GS-1101; Idelalisib)

Cat. No.: HY-13026 Purity: 98.38%
Data Sheet SDS Handling Instructions

CAL-101 is a highly selective and potent p110δ inhibitor with IC50 of 2.5 nM, is 40- to 300-fold more selective for p110δ relative to other PI3K class I enzymes (p110α, p110β, and p110γ; IC50 are 820, 565, and 89nM, respectively).

For research use only. We do not sell to patients.
CAL-101 Chemical Structure

CAL-101 Chemical Structure

CAS No. : 870281-82-6

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10 mM * 1 mL in DMSO $55 In-stock
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    CAL-101 purchased from MCE. Usage Cited in: Br J Haematol. 2015 Jul;170(1):134-8.

    Treatment of CXCR4WT and CXCR4S338X BCWM.1 and MWCL-1 cells with Ibrutinib or Idelalisib induced caspase-3 and PARP cleavage at 6 h. Caspase-3 and PAPR cleavage following Ibrutinib (IB), Idelalisib (ID), ABT-199 (ABT), in the presence of absence of CXCL12 (SDF) and AMD3100 (AMD).

    CAL-101 purchased from MCE. Usage Cited in: Oncotarget. 2016 May 31;7(22):32641-51.

    The well-established PI3Kδ specific inhibitor, CAL-101, shows similar effects as PI3KD-IN-015 with an EC50 of 2.3 nM against PI3Kδ and over 1000-fold less potent against the other three isoforms. Determination of CAL-101 inhibitory activities against PI3Kα, β, δ and γ in cellular background.

    CAL-101 purchased from MCE. Usage Cited in: Patent. US 20160222465 A1.

    Impact of Ibrutinib on p-AKT, ERK and BTK expression following SDF-1a stimulation of plenti-GFP vector, CXCR4WT and CXCR4S338X expressing BCWM.1 cells. plenti-GFP vector, CXCR4WT and CXCR4S338X expressing BCWM.1 cells are pretreated for 2 hours with either Ibrutinib (0.5 uM) or AMD3100 (30 uM) prior to stimulation with SDF-1a (20 nM) for 2 minutes. Results depict differences in phospho-AKT, phospho-ERK, and phospho-BTK obtained by immunoblotting follow

    CAL-101 purchased from MCE. Usage Cited in: Patent. US 20160222465 A1.

    CXCR4S338X expressing BCWM.1 and MWCL-1 cells show variable resistance to PARP and caspase 3 cleavage mediated by WM relevant therapeutics in the presence of SDF-1a, and reversed by AMD3100. plenti-GFP vector, CXCR4WT and CXCR4S338X expressing WM cells are treated for 6 hours with Bendamustine (BENDA), Fludarabine (FLUDARA), Bortezomib (BORT), and Idelalisib (IDELA) at their EC50 doses in the presence or absence of SDF-1a (20 nM) and/or the CXCR4 recep

    CAL-101 purchased from MCE. Usage Cited in: Oncotarget. 2016 Aug 16;7(33):53515-53525.

    PI3KD/V-IN-01 affects autophagy HeLa cells are treated with different concentrations of PI3KD/V-IN-01, VPS34-IN-1, GDC-0941 or CAL-101 for 16 hours before they are fixed and stained for the autophagy marker LC3B.
    • Biological Activity

    • Protocol

    • Technical Information

    • Purity & Documentation

    • References

    Description

    CAL-101 is a highly selective and potent p110δ inhibitor with IC50 of 2.5 nM, is 40- to 300-fold more selective for p110δ relative to other PI3K class I enzymes (p110α, p110β, and p110γ; IC50 are 820, 565, and 89nM, respectively).

    IC50 & Target

    IC50: 2.5 nM (p110δ), 89 nM (p110γ), 565 nM (p110β), 820 nM (p110α)[1]

    In Vitro

    CAL-101 is a highly selective and potent p110δ inhibitor (EC50=8 nM). Greater selectivity (400- to 4000-fold) is seen against related kinases C2β, hVPS34, DNA-PK, and mTOR, whereas no activity is observed against a panel of 402 diverse kinases at 10 μM. CAL-101 reduces PDGF-induced pAkt by only 25% at 10 μM. CAL-101 inhibits LPA-induced pAkt with an EC50 of 1.9 μM. CAL-101 blocks FcϵRI p110δ-mediated CD63 expression with an EC50 of 8 nM, whereas formyl-methionyl-leucyl-phenylalanine activation of p110γ is inhibited with an EC50 of 3 μM. Thus, in cell-based assays, CAL-101 has 240- to 2500-fold selectivity for p110δ over the other class I PI3K isoforms[1]. CAL-101-induced apoptosis of chronic lymphocytic leukemia (CLL) cells is significant compare with vehicle treatment alone (P<0.001). CAL-101 induces selective cytotoxicity in CLL cells independent of IgVH mutational status or interphase cytogenetics[2].

    In Vivo

    A significant reduction is observed in the CD11b+Ly6G+ neutrophils from brain homogenates of bothp110δD910A/D910A mice and CAL-101 (40 mg/kg, i.v.) post-treated mice[3].

    Clinical Trial
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    References
    Preparing Stock Solutions
    Concentration Volume Mass 1 mg 5 mg 10 mg
    1 mM 2.4072 mL 12.0360 mL 24.0720 mL
    5 mM 0.4814 mL 2.4072 mL 4.8144 mL
    10 mM 0.2407 mL 1.2036 mL 2.4072 mL
    Please refer to the solubility information to select the appropriate solvent.
    Cell Assay
    [2]

    CAL-101 is dissolved in DMSO and stored, and then diluted with appropriate media before use[2].

    MTT assays are performed to determine cytotoxicity. Briefly, 1×105 cells (CLL B cells or healthy volunteer T cells or NK cells) are incubated for 48 hours with different concentrations of CAL-101 (0.1 μM, 1 μM, 5 μM, 10 μM), 25 μM LY294002, or vehicle control. MTT reagent is then added, and plates are incubated for an additional 20 hours before washing with protamine sulfate in phosphate-buffered saline. DMSO is added, and absorbance is measured by spectrophotometry at 540 nm in a Labsystems plate reader. Cell viability is also measured at various time points with the use of annexin/PI flow cytometry. Data are analyzed with Expo-ADC32 software package. At least 10,000 cells are counted for each sample. Results are expressed as the percentage of total positive cells over untreated control. Experiments examining caspase-dependent apoptosis included the addition of 100 μM Z-VAD. Experiments examining survival signals include the addition of 1 μg/mL CD40L, 800 U/mL IL-4, 50 ng/mL BAFF, 20 ng/mL TNF-α, or coculturing on fibronectin or stromal (HS-5 cell line) coated plates. Stromal coculture is done by plating a 75-cm2 flask (80%-100% confluent) per 6-well plate 24 hours before the addition of CLL cells[2]. MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Administration
    [3]

    CAL-101 is prepared in DMSO and then diluted[3].

    Mice[3]
    For CAL-101 treatment, wild-type C57BL/6 mice are administered either 40 mg/kg CAL-101 or vehicle DMSO, by 25 μL infusion into the femoral vein, 15 min before I/R (pre-treatment), or 3 and 6 h after initiation of reperfusion (post-treatment). Controls and animals treated with CAL-101 underwent cerebral blood flow (CBF) measurements using a laser Doppler perfusion monitor. The CBF measurements obtained immediately before and after MCAO and again at 3 h after reperfusion showed an ~90-95% reduction in the blood flow to the MCAO infarct region, which does not differ between groups. MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    References
    Molecular Weight

    415.42

    Formula

    C₂₂H₁₈FN₇O

    CAS No.

    870281-82-6

    Storage
    Powder -20°C 3 years
      4°C 2 years
    In solvent -80°C 6 months
      -20°C 1 month
    Shipping

    Room temperature in continental US; may vary elsewhere

    Solvent & Solubility

    DMSO: ≥ 59.7 mg/mL

    * "<1 mg/mL" means slightly soluble or insoluble. "≥" means soluble, but saturation unknown.

    Purity: 98.38%

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    Product Name:
    CAL-101
    Cat. No.:
    HY-13026
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