Bimiralisib hydrochloride
Based on 4 publication(s) in Google Scholar
Bimiralisib hydrochloride (PQR309 hydrochloride) is an orally active, blood-brain barrier-penetrant PI3K/mTOR inhibitor with in vitro antiproliferative activity and in vivo antitumor activity. Bimiralisib hydrochloride induces G1 cell cycle arrest, apoptosis and cell death in cancer cells, while inhibiting cancer cell proliferation, migration, invasion, colony formation and spheroid generation. Bimiralisib hydrochloride upregulates the expression of E2F4. The combination of Bimiralisib hydrochloride with venetoclax enhances therapeutic efficacy in acute myeloid leukemia models. Bimiralisib hydrochloride can be used in cancer-related research.
For research use only. We do not sell to patients.
- CAS No.: 1820902-72-4
- Formula: C17H21ClF3N7O2
- Molecular Weight:447.84
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Publications Citing Use of MedChemExpress (MCE) Bimiralisib hydrochloride
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Biological Activity
Description
IC50 & Target
[4]|
PI3Kα-H1047R 36 nM (IC50) |
PI3Kα-E542K 63 nM (IC50) |
PI3Kα-E545K 136 nM (IC50) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| OCI-Ly1 | IC50 |
1 μM
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Reduction of cell viability in human OCI-Ly1 diffuse large B-cell lymphoma cells assessed by MTT-based kit after 20 h incubation.
Reduction of cell viability in human OCI-Ly1 diffuse large B-cell lymphoma cells assessed by MTT-based kit after 20 h incubation.
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36293442 |
| MOLM-13 | IC50 |
2 μM
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Reduction of cell viability in human MOLM-13 acute myeloid leukemia cells assessed by MTT-based kit after 20 h incubation.
Reduction of cell viability in human MOLM-13 acute myeloid leukemia cells assessed by MTT-based kit after 20 h incubation.
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36293442 |
| ML-2 | IC50 |
3 μM
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Reduction of cell viability in human mL-2 acute myeloid leukemia cells assessed by MTT-based kit after 20 h incubation.
Reduction of cell viability in human mL-2 acute myeloid leukemia cells assessed by MTT-based kit after 20 h incubation.
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36293442 |
| SKM-1 | IC50 |
3 μM
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Reduction of cell viability in human SKM-1 acute myeloid leukemia cells assessed by MTT-based kit after 20 h incubation.
Reduction of cell viability in human SKM-1 acute myeloid leukemia cells assessed by MTT-based kit after 20 h incubation.
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36293442 |
| HL-60 | IC50 |
5 μM
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Reduction of cell viability in human HL-60 acute myeloid leukemia cells assessed by MTT-based kit after 20 h incubation.
Reduction of cell viability in human HL-60 acute myeloid leukemia cells assessed by MTT-based kit after 20 h incubation.
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36293442 |
| OCI-AML-3 | IC50 |
10 μM
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Reduction of cell viability in human OCI-AML3 acute myeloid leukemia cells assessed by MTT-based kit after 20 h incubation.
Reduction of cell viability in human OCI-AML3 acute myeloid leukemia cells assessed by MTT-based kit after 20 h incubation.
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36293442 |
| MOLM-16 | IC50 |
10 μM
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Reduction of cell viability in human MOLM-16 acute myeloid leukemia cells assessed by MTT-based kit after 20 h incubation.
Reduction of cell viability in human MOLM-16 acute myeloid leukemia cells assessed by MTT-based kit after 20 h incubation.
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36293442 |
| AGS | IC50 |
0.611 μM
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Antiproliferative activity against human AGS gastric cancer cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
Antiproliferative activity against human AGS gastric cancer cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay.
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42414236 |
In Vitro
Bimiralisib hydrochloride inhibits the proliferation and induces apoptosis of human glioblastoma U87 and U251 cells, reduces the migration and invasion abilities of glioma cells, and also induces G1-phase cell cycle arrest in a dose-dependent manner[1].
Bimiralisib (PQR-309) hydrochloride reduces the viability of OCI-Ly1 diffuse large B-cell lymphoma (DLBCL) cells, MOLM-13 acute myeloid leukemia (AML) cells, mL-2 and SKM-1 AML cells, HL-60 AML cells, as well as OCI-AML3, PL-21 and MOLM-16 AML cells, with corresponding IC50 values of 1 μM, 2 μM, 3 μM, 5 μM and 10 μM[2].
Bimiralisib (1 μM alone or combined with 100 nM Venetoclax (HY-15531); 20 h) hydrochloride exhibits reduced cytotoxic potency in MOLM-13, SKM-1 and OCI-AML3 acute myeloid leukemia (AML) cells due to the protective effect of bone marrow stroma[2].
Bimiralisib (0.312-20.0 μM; 72 h) hydrochloride potently inhibits the viability of human gastric cancer cell lines SNU-484, SNU-668 and AGS, with IC50 values of 0.792 μM, 0.419 μM and 0.611 μM, respectively[3].
Bimiralisib (0.312-1.25 μM; 8 days) hydrochloride inhibits clonogenic growth of SNU-484, SNU-668 and AGS human gastric cancer cells[3].
Bimiralisib (0.312-1.25 μM; 14 days) hydrochloride inhibits the anchorage-independent sphere growth of SNU-484, SNU-668 and AGS human gastric cancer cells[3].
Bimiralisib (0.625-1.25 μM; 24 h) hydrochloride effectively inhibits the PI3K/mTOR signaling pathway in SNU-484 and AGS human gastric cancer cells by reducing the phosphorylation levels of AKT, mTOR and p70S6K. It also induces G1-phase cell cycle arrest in SNU-484 and AGS human gastric cancer cells and regulates the expression of G1-phase cell cycle regulatory proteins, specifically characterized by upregulated expression of E2F4, p107 and (in AGS cells) p21, and downregulated expression of Cyclin E[3].
Bimiralisib (0.625-1.25 μM; 48 h) hydrochloride inhibits the migratory capacity of human gastric cancer cells SNU-484 and AGS under low-serum (1% FBS) conditions; it regulates the expression of epithelial-mesenchymal transition-related markers in human gastric cancer cells SNU-484 and AGS, upregulating E-cadherin expression and downregulating vimentin expression[3].
Bimiralisib hydrochloride has IC50 values of 36 nM, 63 nM and 136 nM for PI3Kα-H1047R, PI3Kα-E542K and PI3Kα-E545K, respectively[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:Susceptible AML cell lines (MOLM-13, mL-2, SKM-1, OCI-AML3), HS-5 bone marrow stroma cells
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Concentration:1 μM alone or in combination with 100 nM Venetoclax
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Incubation Time:20 h
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Result:Reduced cytotoxic efficacy in AML cells due to bone marrow stroma protection: MOLM-13 cells were protected against the combination treatment.
SKM-1 cells were protected against bimiralisib single-agent and combination treatment.
mL-2 cells showed no specific protection against bimiralisib-containing treatments.
OCI-AML3 cells were protected against all venetoclax combination treatments including with bimiralisib.
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Cell Line:human gastric cancer cell lines SNU-484, SNU-668, AGS
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Concentration:0.312, 0.625, 1.25, 2.5, 5, 10, 20 μM
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Incubation Time:72 h
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Result:Reduced cell viability in a dose-dependent manner across all three cell lines.
Achieved IC50 values of 0.792 μM for SNU-484, 0.419 μM for SNU-668, and 0.611 μM for AGS cells.
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Cell Line:human gastric cancer cell lines SNU-484, SNU-668, AGS
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Concentration:0.312, 0.625, 1.25 μM
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Incubation Time:8 days
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Result:Suppressed clonogenic growth of SNU-484, SNU-668, and AGS human gastric cancer cells.
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Cell Line:human gastric cancer cell lines SNU-484, AGS
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Concentration:0.625, 1.25 μM
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Incubation Time:24 h
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Result:Markedly reduced phosphorylation of AKT (S473), mTOR (S2448), and p70S6K (T389) in both SNU-484 and AGS cells.
Left total levels of AKT and mTOR unchanged.\nIncreased expression of E2F4 and p107 in both cell lines.
Decreased Cyclin E expression in both cell lines.
Increased p21 expression in AGS cells, while p21 was barely detectable in SNU-484 cells.
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Cell Line:human gastric cancer cell lines SNU-484, AGS
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Concentration:0.625, 1.25 μM
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Incubation Time:24 h
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Result:Caused a significant accumulation of cells in the G1 phase in both SNU-484 and AGS cells.
Induced a corresponding decrease in the S phase population in both SNU-484 and AGS cells.
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Cell Line:human gastric cancer cell lines SNU-484, AGS
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Concentration:0.625, 1.25 μM
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Incubation Time:48 h (1% FBS medium)
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Result:Significantly delayed wound closure in a dose-dependent manner in both SNU-484 and AGS cells compared to untreated controls.
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Cell Line:human gastric cancer cell lines SNU-484, AGS
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Concentration:0.625, 1.25 μM
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Incubation Time:48 h (1% FBS medium)
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Result:Caused a dose-dependent increase in E-cadherin expression in both SNU-484 and AGS cells.
Induced a dose-dependent decrease in vimentin expression in both SNU-484 and AGS cells.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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CAS No. 1820902-72-4
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Molecular Weight 447.84
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Formula C17H21ClF3N7O2
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SMILES
FC(F)(C1=CC(N)=NC=C1C2=NC(N3CCOCC3)=NC(N4CCOCC4)=N2)F.Cl
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Synonyms
PQR309 hydrochloride
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (4)
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Journal Impact Factor
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Most Recent
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Leukemia
BET inhibitor-based combinations targeting novel dependencies in MECOM-rearranged (r) AML. [Abstract]2025 Dec 19. PMID: 41419608 -
Int J Mol Sci
Rationale for Combining the BCL2 Inhibitor Venetoclax with the PI3K Inhibitor Bimiralisib in the Treatment of IDH2- and FLT3-Mutated Acute Myeloid Leukemia. [Abstract]2022 Oct 20;23(20):12587. PMID: 36293442 -
Front Pharmacol
CC-223, NSC781406, and BGT226 Exerts a Cytotoxic Effect Against Pancreatic Cancer Cells via mTOR Signaling. [Abstract]2020 Nov 11:11:580407. PMID: 33343350 -
Eur J Immunol
Fibroblast transdifferentiation promotes conversion of M1 macrophages and replenishment of cardiac resident macrophages following cardiac injury in mice. [Abstract]2020 Jun;50(6):795-808. PMID: 32068249
Purity & Documentation
References
[2]. Seipel K, et al. Rationale for Combining the BCL2 Inhibitor Venetoclax with the PI3K Inhibitor Bimiralisib in the Treatment of IDH2- and FLT3-Mutated Acute Myeloid Leukemia. International journal of molecular sciences. 2022 Oct 20;23(20):12587. [Content Brief]
[3]. Noh YJ, et al. Bimiralisib suppresses proliferation and migration of gastric cancer cells PI3K/mTOR pathway inhibition. The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology. 2026 Jul 08. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Bimiralisib hydrochloride Related Classifications
HY-12868A Related Classifications
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