WARNING: This product is for research use only, not for human or veterinary use.

MedKoo CAT#: 205710

CAS#: 1025065-69-3

Description: SGI-1776 is a small-molecule pan-Pim protein kinase inhibitor with potential antineoplastic activity. Pim kinase inhibitor SGI-1776 binds to and inhibits the activities of Pim-1, -2 and -3, serine-threonine kinases, which may result in the interruption of the G1/S phase cell cycle transition, the expression of pro-apoptotic Bcl2 proteins and tumor cell apoptosis. PIM kinases play key roles in cell cycle progression and apoptosis inhibition and may be overexpressed in various malignancies.

Chemical Structure

CAS# 1025065-69-3

Theoretical Analysis

MedKoo Cat#: 205710
Name: SGI-1776
CAS#: 1025065-69-3
Chemical Formula: C20H22F3N5O
Exact Mass: 405.17764
Molecular Weight: 405.42
Elemental Analysis: C, 59.25; H, 5.47; F, 14.06; N, 17.27; O, 3.95

Size Price Shipping out time Quantity
10mg USD 150 Same day
25mg USD 250 Same day
50mg USD 450 Same day
100mg USD 850 Same day
200mg USD 1350 Same day
500mg USD 2150 2 Weeks
1g USD 2950 2 Weeks
2g USD 5250 2 Weeks
5g USD 7450 2 Weeks
Inquire bulk and customized quantity

Pricing updated 2021-03-03. Prices are subject to change without notice.

SGI-1776, purity > 98%, is in stock. The same day shipping out after order is received.

Synonym: SGI1776; SGI-1776; SGI 1776.

IUPAC/Chemical Name: N-((1-methylpiperidin-4-yl)methyl)-3-(4-(trifluoromethoxy)phenyl)imidazo[1,2-b]pyridazin-6-amine.


InChi Code: InChI=1S/C20H22F3N5O/c1-27-10-8-14(9-11-27)12-24-18-6-7-19-25-13-17(28(19)26-18)15-2-4-16(5-3-15)29-20(21,22)23/h2-7,13-14H,8-12H2,1H3,(H,24,26)


white solid powder

>98% (or refer to the Certificate of Analysis)

Shipping Condition:
Shipped under ambient temperature as non-hazardous chemical. This product is stable enough for a few weeks during ordinary shipping and time spent in Customs.

Storage Condition:
Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).

Soluble in DMSO, not in water

Shelf Life:
>2 years if stored properly

Drug Formulation:
This drug may be formulated in DMSO

Stock Solution Storage:
0 - 4 C for short term (days to weeks), or -20 C for long term (months).

HS Tariff Code:

Preparing Stock Solutions

The following data is based on the product molecular weight 405.42 Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.

Select a batch to recalculate based on the batch molecular weight:
Concentration / Solvent Volume / Mass 1 mg 5 mg 10 mg
1 mM 1.15 mL 5.76 mL 11.51 mL
5 mM 0.23 mL 1.15 mL 2.3 mL
10 mM 0.12 mL 0.58 mL 1.15 mL
50 mM 0.02 mL 0.12 mL 0.23 mL

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1: Siu A, Virtanen C, Jongstra J. PIM kinase isoform specific regulation of MIG6 expression and EGFR signaling in prostate cancer cells. Oncotarget. 2011 Dec 22. [Epub ahead of print] PubMed PMID: 22193779.

2: Batra V, Maris JM, Kang MH, Reynolds CP, Houghton PJ, Alexander D, Kolb EA, Gorlick R, Keir ST, Carol H, Lock R, Billups CA, Smith MA. Initial testing (stage 1) of SGI-1776, a PIM1 kinase inhibitor, by the pediatric preclinical testing program. Pediatr Blood Cancer. 2011 Nov 2. doi: 10.1002/pbc.23364. [Epub ahead of print] PubMed PMID: 22052829.

3: Mahalingam D, Espitia CM, Medina EC, Esquivel JA 2nd, Kelly KR, Bearss D, Choy G, Taverna P, Carew JS, Giles FJ, Nawrocki ST. Targeting PIM kinase enhances the activity of sunitinib in renal cell carcinoma. Br J Cancer. 2011 Nov 8;105(10):1563-73. doi: 10.1038/bjc.2011.426. Epub 2011 Oct 20. PubMed PMID: 22015557; PubMed Central PMCID: PMC3242528.

4: Chen LS, Redkar S, Taverna P, Cortes JE, Gandhi V. Mechanisms of cytotoxicity to Pim kinase inhibitor, SGI-1776, in acute myeloid leukemia. Blood. 2011 Jul 21;118(3):693-702. Epub 2011 May 31. PubMed PMID: 21628411; PubMed Central PMCID: PMC3142906.

5: Chang M, Kanwar N, Feng E, Siu A, Liu X, Ma D, Jongstra J. PIM kinase inhibitors downregulate STAT3(Tyr705) phosphorylation. Mol Cancer Ther. 2010 Sep;9(9):2478-87. Epub 2010 Jul 28. PubMed PMID: 20667852.

6: Mumenthaler SM, Ng PY, Hodge A, Bearss D, Berk G, Kanekal S, Redkar S, Taverna P, Agus DB, Jain A. Pharmacologic inhibition of Pim kinases alters prostate cancer cell growth and resensitizes chemoresistant cells to taxanes. Mol Cancer Ther. 2009 Oct;8(10):2882-93. PubMed PMID: 19825806; PubMed Central PMCID: PMC2808126.

7: Chen LS, Redkar S, Bearss D, Wierda WG, Gandhi V. Pim kinase inhibitor, SGI-1776, induces apoptosis in chronic lymphocytic leukemia cells. Blood. 2009 Nov 5;114(19):4150-7. Epub 2009 Sep 4. PubMed PMID: 19734450; PubMed Central PMCID: PMC2774551.

Additional Information

SGI-1776: results from the pediatric preclinical testing program. Researchers from Children's Hospital of Philadelphia recently reported that SGI-1776 exhibited cytotoxic activity in vitro with a median relative IC(50) of 3.1 µM. SGI-1776 induced significant differences in EFS distribution in vivo in 9 of 31 solid tumor xenografts and in 1 of 8 of the evaluable ALL xenografts. SGI-1776 induced tumor growth inhibition meeting criteria for intermediate EFS T/C activity in 1 of 39 evaluable models. In contrast, SGI-1776 induced complete responses of subcutaneous MV4;11 (B myeloid leukemia). (source: Pediatr Blood Cancer. 2011 Nov 2. doi: 10.1002/pbc.23364. [Epub ahead of print] )
Mechanisms of cytotoxicity: SGI-1776  in acute myeloid leukemia. Chen et al recently report that treatment of AML cells with SGI-1776 resulted  in a concentration-dependent induction of apoptosis and we investigated its effect on Pim kinase functions. Phosphorylation of traditional Pim kinase targets, c-Myc(Ser62) and 4E-BP1 (Thr36/Thr47), were both decreased in actively cycling AML cell lines MV-4-11, MOLM-13 and OCI-AML-3. Levels of antiapoptotic proteins Bcl-2, Bcl-x(L), XIAP, and proapoptotic Bak and Bax were unchanged; however, a significant reduction in Mcl-1 was observed. This was correlated with inhibition of global RNA and protein synthesis and MCL-1 transcript decline after SGI-1776 treatment. These data suggest that SGI-1776 mechanism in AML involves Mcl-1 protein reduction. Consistent with cell line data, xenograft model studies with mice bearing MV-4-11 tumors showed efficacy with SGI-1776 . Importantly, SGI-1776 was also cytotoxic in AML primary cells, irrespective of FLT3 mutation status and resulted in Mcl-1 protein decline.  (source: Blood. 2011 Jul 21;118(3):693-702. Epub 2011 May 31 .)