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SGI-1776

Name: SGI-1776
Brand: MedChemExpress
SKU: HY-13287A
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12 Cited Publications

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Based on 12 publication(s) in Google Scholar

SGI-1776 is an orally active Pim kinase and FLT3 inhibitor with IC₅₀ values of 7 nM, 363 nM, 69 nM, and 44 nM for Pim-1, Pim-2, Pim-3, and FLT3, respectively. SGI-1776 downregulates C/EBP-α, PPAR-γ, FAS, Leptin, and RANTES, and decreases STAT-3 phosphorylation. SGI-1776 induces Apoptosis, cell cycle arrest, mitochondrial depolarization, and reduces RNA synthesis, protein synthesis, and Mcl-1. SGI-1776 inhibits adipogenesis and lipid accumulation. SGI-1776 has anticancer activity against leukemia.

For research use only. We do not sell to patients.

CAS No.: 1173928-26-1
Formula: C₂₀H₂₆F₃N₅O₉S₂
Molecular Weight:601.57

Storage:

Please store the product under the recommended conditions in the Certificate of Analysis.

Data Sheet (296 KB)

SGI-1776 Chemical Structure

CAS No.: 1173928-26-1

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Use of MCE Products

Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Publications (12)
Purity & Documentation
References
Calculators
Help & FAQs
Classifications
Bioz

Biological Activity

Description

IC₅₀ & Target

^[1]^[2]

Mcl-1

PIM1

7 nM (IC₅₀)

PIM2

363 nM (IC₅₀)

PIM3

69 nM (IC₅₀)

PPAR-γ

Stat-3

All Pim Isoforms :

All PPAR Isoforms :

All STAT Isoforms :

All DNA/RNA Synthesis Isoforms :

All Bcl-2 Family Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
MOLM-13	IC50	10 nM	Viability IC50 of less than 10 nM against human FLT3-ITD AML cell line MOLM-13 after 72 hrs incubation with SGI-1776, associated with apoptosis induction. Viability IC50 of less than 10 nM against human FLT3-ITD AML cell line MOLM-13 after 72 hrs incubation with SGI-1776, associated with apoptosis induction.	561980
MV4-11	IC50	10 nM	Viability IC50 of less than 10 nM against human FLT3-ITD AML cell line MV4-11 after 72 hrs incubation with SGI-1776, associated with apoptosis induction. Viability IC50 of less than 10 nM against human FLT3-ITD AML cell line MV4-11 after 72 hrs incubation with SGI-1776, associated with apoptosis induction.	561980
JeKo-1	IC50	5 μM	Inhibition of RNA synthesis in human mantle cell lymphoma Jeko cells assessed by uridine incorporation with 50% reduction after exposure to SGI-1776. Inhibition of RNA synthesis in human mantle cell lymphoma Jeko cells assessed by uridine incorporation with 50% reduction after exposure to SGI-1776.	24290221
Mino	IC50	10 μM	Inhibition of RNA synthesis in human mantle cell lymphoma Mino cells assessed by uridine incorporation with 50% reduction after exposure to SGI-1776. Inhibition of RNA synthesis in human mantle cell lymphoma Mino cells assessed by uridine incorporation with 50% reduction after exposure to SGI-1776.	24290221

In Vitro

Anti-cancerApoptosisCell Cycle RegulationLipid MetabolismCytokines & ChemokinesMitochondrial FunctionOthers

Anti-cancer

SGI-1776 (0.1-10 µM; 24 h) inhibits global RNA synthesis in MV-4-11, MOLM-13, and OCI-AML-3 AML cell lines in a dose-dependent manner^[2].
SGI-1776 (3-10 µM; 24 h) inhibits clonogenic survival of MV-4-11 cells, reducing colony formation to approximately 5% of control at 10 µM^[2].
SGI-1776 (2.5-5 μM; 72 h) reduces colony formation in SACC-83 and SACC-LM cells^[3].
SGI-1776 inhibits the proliferation of mouse ALL and hALL cell lines, with IC₅₀ values of approximately 1 mM and 2.5 mM, respectively^[5].

Anti-cancer

Apoptosis

SGI-1776 (0.1-10 µM; 24 hours) induces dose-dependent apoptosis in MV-4-11, MOLM-13, and OCI-AML-3 AML cell lines^[2].
SGI-1776 (0.1-10 µM; 24 hours) selectively reduces Mcl-1 protein levels in MV-4-11, MOLM-13, and OCI-AML-3 AML cell lines without altering Bcl-2, Bcl-xL, Bak, or Bax^[2].
SGI-1776 reduces the viability and clonogenic survival of 9 hAML cell lines, inhibits proliferation and induces apoptosis, while decreasing Bad phosphorylation and increasing p27 expression^[7].
SGI-1776 (1-10 μM; 24 h) induces apoptosis in primary AML cells, with an average increase of 5-19%^[8].

Apoptosis

SGI-1776 (2.5-5 μM; 72 h) reduces Pim-1, p-FOXO3a, RUNX3, Bcl-2, p-BAD, and p-Bim protein levels in SACC-83 and SACC-LM cells^[3].
SGI-1776 (2.5-5 μM; 72 h) induces early apoptosis in SACC-83 and SACC-LM cells in a dose-dependent manner^[3].
SGI-1776 (2.5-5 μM; 72 h) increases caspase-3 activity in SACC-83 and SACC-LM cells, with higher activity in SACC-LM cells^[3].

Cell Cycle Regulation

SGI-1776 (2.5-5 μM; 72 hours) reduces BrdU incorporation in SACC-83 and SACC-LM cells^[3].
SGI-1776 (2.5-5 μM; 72 h) induces G0/G1 and G2/M cell cycle arrest in SACC-83 and SACC-LM cells and reduces the proportion of cells in S phase^[3].

Lipid Metabolism

SGI-1776 (5-10 µM; 8 days of differentiation) inhibits lipid droplet accumulation in differentiating 3T3-L1 adipocytes, with 10 µM completely blocking lipid droplets and 5 µM producing significant inhibition^[1].
SGI-1776 (5-10 µM; 8 days of differentiation) reduces triglyceride content in differentiating 3T3-L1 adipocytes, with the greatest reduction at 10 µM and activity at 5 µM^[1].
SGI-1776 (5-10 µM; 8-day differentiation) does not significantly reduce 3T3-L1 adipocyte viability at 5 µM after 8 days, whereas 10 µM causes a slight decrease^[1].
SGI-1776 (5 µM; days 0-8) inhibits 3T3-L1 adipogenesis mainly when present during the early differentiation stage, and incubation on days 0-8 produces the highest inhibition rate^[1].

Lipid Metabolism

Cytokines & Chemokines

SGI-1776 (5 µM; days 2-8 and 2-24 hours) downregulates C/EBP-α, PPAR-γ, and FAS protein expression in differentiating 3T3-L1 adipocytes and inhibits STAT-3 phosphorylation^[1].

Mitochondrial Function

SGI-1776 (2.5-5 μM; 72 h) induces mitochondrial depolarization^[3].

Others

SGI-1776 (IC₅₀ = 7 nM for Pim-1; IC₅₀ = 363 nM for Pim-2; IC₅₀ = 69 nM for Pim-3; IC₅₀ = 44 nM for FLT3) is a biochemical inhibitor of Pim-1, Pim-2, Pim-3, and FLT3 kinases^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Differentiation Assay^[1]

Cell Line:

3T3-L1 preadipocytes differentiated into mature adipocytes
Concentration:

5 and 10 µM
Incubation Time:

8-day differentiation
Result:

SGI-1776 for 8 days markedly reduced lipid droplets in a concentration-dependent manner compared with mock control cells.
10 µM SGI-1776 completely blocked accumulation of lipid droplets.
Light microscopy confirmed the SGI-1776-mediated lipid-reducing effect.
SGI-1776 at 5 and 10 µM reduced Oil Red O staining relative to control.

Cell Viability Assay^[1]

Cell Line:

3T3-L1 adipocytes
Concentration:

5 and 10 µM
Incubation Time:

8-day differentiation
Result:

Induced a slight decrease in viability at 10 µM, but not at 5 µM.
SGI-1776 at 5 µM for 8 days did not markedly affect the number of 3T3-L1 adipocytes.

Western Blot Analysis^[1]

Cell Line:

3T3-L1 preadipocytes/adipocytes
Concentration:

5 µM
Incubation Time:

days 2, 5, 8 during differentiation; 2, 4, 8, 24 h after MDI induction
Result:

Markedly inhibited adipogenesis-dependent protein expression of C/EBP-α and PPAR-γ during adipocyte differentiation, particularly on days 5 and 8.
Markedly decreased phosphorylation levels of STAT-3 on day 2 during adipocyte differentiation.
Did not markedly affect phosphorylation levels of STAT-5.
Suppressed STAT-3 phosphorylation during early stages of adipogenesis induced by MDI at 2, 4, 8 and 24 h.
Did not markedly alter total protein levels of STAT-3 and STAT-5 during adipocyte differentiation.
Markedly suppressed FAS protein expression on days 5 and 8.

Apoptosis Analysis^[2]

Cell Line:

MV-4-11, MOLM-13, and OCI-AML-3
Concentration:

0.1, 0.3, 1, 3, 10 µM; DMSO vehicle control
Incubation Time:

24 h
Result:

Induced a dose-dependent increase in annexin/PI-positive cells in MV-4-11, MOLM-13, and OCI-AML-3 cells.
In MV-4-11, annexin/PI-positive cells were 6% at 0 µM, 6% with DMSO, 13% at 0.1 µM, 20% at 0.3 µM, 26% at 1 µM, 28% at 3 µM, and 75% at 10 µM.
MOLM-13 and OCI-AML-3 showed dose-dependent increases in annexin/PI-positive cells.
Higher apoptosis occurred in MV-4-11 and MOLM-13, which are FLT3-ITD positive.

In Vivo

Anti-cancer

SGI-1776 (50-200 mg/kg; oral; 5 days per week daily or twice weekly; 3 weeks) is effective in the MV-4-11 AML xenograft mouse model, producing complete tumor regression at 75 mg/kg daily and 200 mg/kg twice weekly, with T/C values of 13% and 11% at 50 mg/kg daily and 100 mg/kg twice weekly, respectively^[2].
SGI-1776 (200 mg/kg/dose; oral; daily × 5 per week) shows in vivo activity in ALL xenografts, reducing tumor proliferation compared with untreated mice^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

NOD-SCID (female)^[2]
Dosage:

50 mg/kg (daily 5 days/week for 3 weeks); 75 mg/kg (daily 5 days/week for 3 weeks); 100 mg/kg (twice weekly for 3 weeks); 200 mg/kg (twice weekly for 3 weeks)
Administration:

p.o.; daily 5 days/week for 3 weeks (50, 75 mg/kg); twice weekly for 3 weeks (100, 200 mg/kg)
Result:

In MV-4-11 xenografts, oral SGI-1776 produced potent and sustained antitumor activity.
Tumors in the 75 mg/kg and 200 mg/kg groups disappeared or became almost impalpable within 1 week after administration.
On day 22, 8 of 9 mice given 75 mg/kg SGI-1776 and all 10 mice given 200 mg/kg experienced complete regression; 3 mice in the 75 mg/kg group and 1 mouse in the 200 mg/kg group experienced minor regrowth by the end of the observation period.
Administration of 50 mg/kg SGI-1776 on a daily schedule or 100 mg/kg on a twice-weekly schedule resulted in some antitumor effect; no regressions were observed on day 18, but T/C was 13% after 50 mg/kg and 11% after 100 mg/kg on day 22.
Potent efficacy was achieved with an intermittent dosing schedule (2 oral doses/week) at 100 or 200 mg/kg.

Animal Model:

NOD/SCID^[5]
Dosage:

200 mg/kg/dose; 100 mg/kg/dose (survival studies)
Administration:

gavage; daily ×5 per week
Result:

Alone or with rapamycin decreased in vivo tumor proliferation over time compared with untreated mice.
At 200 mg/kg/dose, no difference in survival could be detected.
Survival studies at 100 mg/kg/dose were ongoing.

Related Protocols :

Chemical Information

CAS No. 1173928-26-1
Molecular Weight 601.57
Formula C₂₀H₂₆F₃N₅O₉S₂
SMILES

CN1CCC(CC1)CNC2=NN3C(C=C2)=NC=C3C4=CC=CC(OC(F)(F)F)=C4.O=S(O)(O)=O.O=S(O)(O)=O
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Publications (12)

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Journal Impact Factor

Science

The target landscape of clinical kinase drugs. [Abstract]

2017 Dec 1;358(6367):eaan4368. PMID: 29191878
Sci Transl Med

PP2A inhibition is a druggable MEK inhibitor resistance mechanism in KRAS-mutant lung cancer cells. [Abstract]

2018 Jul 18;10(450):eaaq1093. PMID: 30021885
Adv Sci (Weinh)

PIM1 Attenuates Innate Immunity to Foster Coronavirus Replication through Ubiquitin Ligase β-TrCP-Mediated IFNAR1 Degradation. [Abstract]

2025 Jul 6:e03487. PMID: 40619619
Cell Death Dis

PIM1 mediates epithelial-mesenchymal transition by targeting Smads and c-Myc in the nucleus and potentiates clear-cell renal-cell carcinoma oncogenesis. [Abstract]

2018 Feb 22;9(3):307. PMID: 29472550

SGI-1776 purchased from MedChemExpress. Usage Cited in: Cell Death Dis. 2018 Feb 22;9(3):307. [Abstract]

PIM1 directly phosphorylated Smad2 and Smad3 and that inhibition of PIM1 kinase activity with SGI-1776 significantly reduces the protein levels of p-Smad2 and p-Smad3
Phytomedicine

6''-O-acetylsaikosaponin D targets STAT3-mediated transcriptional remodeling to induce ferroptosis and apoptosis. [Abstract]

2026 May 15:157:158301. PMID: 42166974
Cell Chem Biol

PIM1 targeted degradation prevents the emergence of chemoresistance in prostate cancer. [Abstract]

2024 Feb 15;31(2):326-337.e11. PMID: 38016478
J Med Chem

Discovery of a Dual Tubulin and Poly(ADP-Ribose) Polymerase-1 Inhibitor by Structure-Based Pharmacophore Modeling, Virtual Screening, Molecular Docking, and Biological Evaluation. [Abstract]

2021 Nov 11;64(21):15702-15715. PMID: 34670362
Front Cell Infect Microbiol

ZIKV prM hijacks PIM1 kinase for phosphorylation to prevent ubiquitin-mediated degradation and facilitate viral replication. [Abstract]

2024 Nov 29:14:1502770. PMID: 39679197
Food Chem Toxicol

2026 Nov:217:116309. PMID: 42537713
eNeuro

PIM-Related Kinases Selectively Regulate Olfactory Sensations in Caenorhabditis elegans. [Abstract]

2019 Aug 22;6(4):ENEURO.0003-19.2019. PMID: 31387876
Anticancer Drugs

AZD7762 induces CRBN dependent BAG3 degradation through ubiquitin-proteasome pathway. [Abstract]

2024 Jan 1;35(1):46-54. PMID: 37449977
Patent

US20180263995A1.

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (296 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[1]. Park YK, et al. The novel anti-adipogenic effect and mechanisms of action of SGI-1776, a Pim-specific inhibitor, in 3T3-L1 adipocytes. International Journal of Molecular Medicine. 2016 Jan 1;37(1):157-64. [Content Brief]

[2]. Chen LS, et al. Mechanisms of cytotoxicity to Pim kinase inhibitor, SGI-1776, in acute myeloid leukemia. Blood. 2011 Jul 21;118(3):693-702. [Content Brief]

[3]. Hou X, et al. Biochemical changes of salivary gland adenoid cystic carcinoma cells induced by SGI-1776. Experimental cell research. 2017 Mar 15;352(2):403-411. [Content Brief]

[4]. Chen Q, et al. The Mechanisms of PIM Kinase Inhibitor, SGI-1776 Free Base, in Treating Myeloma-Associated Bone Disease. Blood. 2017 Dec 8;130:3079.

[5]. Brown VI, et al. Inhibiting PIM-1 Is Effective in Vitro and in Vivo against ALL: A Novel Mechanistic and Potentially Clinically Relevant Druggable Target. Blood. 2008 Nov 16;112(11):1922.

[6]. Lampron MC, et al. Pim1: A New Dna Repair Modulator Implicated in Pulmonary Hypertension. Circulation. 2017 Nov 14;136(suppl_1):A16978-.

[7]. Kelly KR, et al. Targeting PIM kinase activity with the novel small molecule inhibitor SGI-1776 significantly augments the efficacy of cytarabine in models of acute myeloid leukemia. Blood. 2010 Nov 19;116(21):3253.

[8]. Chen LS, et al. Pim kinase inhibitor, SGI-1776, induces apoptosis in acute myeloid leukemia primary cells. Cancer Research. 2010 Apr 15;70(8_Supplement):1649-.

[9]. Yang Q, et al. Targeting Pim kinases by SGI-1776 in mantle cell lymphoma. Cancer Research. 2011 Apr 15;71(8_Supplement):586-.

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SGI-1776

Publications Citing Use of MedChemExpress (MCE) SGI-1776

All Pim Isoforms

All PPAR Isoforms

All STAT Isoforms

All DNA/RNA Synthesis Isoforms

All Bcl-2 Family Isoforms