WARNING: This product is for research use only, not for human or veterinary use.
MedKoo CAT#: 406610
CAS#: 1423715-09-6
Description: SP-2509 is a novel histone demethylase LSD1 inhibitor, which showed high actitivity on human AML cells. Treatment with the novel LSD1 antagonist SP2509 attenuated the binding of LSD1 with the corepressor CoREST, increased the permissive H3K4Me3 mark on the target gene promoters, and increased the levels of p21, p27 and CCAAT/enhancer binding protein α in cultured AML cells. In addition, SP2509 treatment or LSD1 shRNA inhibited the colony growth of AML cells.
MedKoo Cat#: 406610
Name: SP-2509
CAS#: 1423715-09-6
Chemical Formula: C19H20ClN3O5S
Exact Mass: 437.08122
Molecular Weight: 437.9
Elemental Analysis: C, 52.11; H, 4.60; Cl, 8.10; N, 9.60; O, 18.27; S, 7.32
Synonym: SP2509; SP 2509; SP-2509.
IUPAC/Chemical Name: (E)-N'-(1-(5-chloro-2-hydroxyphenyl)ethylidene)-3-(morpholinosulfonyl)benzohydrazide.
InChi Key: NKUDGJUBIVEDTF-FYJGNVAPSA-N
InChi Code: InChI=1S/C19H20ClN3O5S/c1-13(17-12-15(20)5-6-18(17)24)21-22-19(25)14-3-2-4-16(11-14)29(26,27)23-7-9-28-10-8-23/h2-6,11-12,24H,7-10H2,1H3,(H,22,25)/b21-13+
SMILES Code: O=C(N/N=C(C1=CC(Cl)=CC=C1O)\C)C2=CC=CC(S(=O)(N3CCOCC3)=O)=C2
Appearance: Solid powder
Purity: >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).
Solubility: 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: 2934.99.9001
| Biological target: | SP2509 is a potent and selective antagonist of lysine specific demethylase 1 (LSD1) with an IC50 of 13 nM. |
| In vitro activity: | Treatment with the novel LSD1 antagonist SP2509 attenuated the binding of LSD1 with the corepressor CoREST, increased the permissive H3K4Me3 mark on the target gene promoters, and increased the levels of p21, p27 and CCAAT/enhancer binding protein α in cultured AML cells. In addition, SP2509 treatment or LSD1 shRNA inhibited the colony growth of AML cells. SP2509 also induced morphological features of differentiation in the cultured and primary AML blasts. SP2509 induced more apoptosis of AML cells expressing mutant NPM1 than mixed-lineage leukemia fusion oncoproteins. Reference: Leukemia. 2014 Nov;28(11):2155-64. https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24699304/ |
| In vivo activity: | The in vivo anti-AML activity of SP2509 in NOD/SCID mice, as well as against primary AML blasts engrafted in the bone marrow, i.e., ‘primagrafts’ in the NSG mice was examined. Following the tail vein infusion and engraftment of OCI-AML3 cells, the effect of the treatment with the vehicle control or SP2509 alone for 3 weeks on the survival of the NOD/SCID mice was determined. The Kaplan Meier plot depicting the survival of the mice demonstrates that, as compared to treatment with the vehicle alone, treatment with SP2509 significantly improved the median survival of the mice infused with OCI-AML3 cells (37 and 36.5 days, respectively, versus 19.5 days for vehicle control) (p < 0.05) (Figure 7D). Figure 7E demonstrates the effects of SP2509 on the survival of NSG mice engrafted with the primary AML blasts co-expressing FLT3-ITD and NPM1c+. As shown, treatment with SP2509 for 3 weeks significantly improved the median survival of the mice, as compared to the treatment with vehicle control (p < 0.01). Reference: Leukemia. 2014 Nov;28(11):2155-64. https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24699304/ |
| Solvent | Max Conc. mg/mL | Max Conc. mM | |
|---|---|---|---|
| Solubility | |||
| DMSO | 33.0 | 75.36 |
The following data is based on the product molecular weight 437.9 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.
| 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 |
| In vitro protocol: | 1. Fiskus W, Sharma S, Shah B, Portier BP, Devaraj SG, Liu K, Iyer SP, Bearss D, Bhalla KN. Highly effective combination of LSD1 (KDM1A) antagonist and pan-histone deacetylase inhibitor against human AML cells. Leukemia. 2014 Nov;28(11):2155-64. doi: 10.1038/leu.2014.119. Epub 2014 Apr 4. Erratum in: Leukemia. 2017 Jul;31(7):1658. PMID: 24699304; PMCID: PMC4739780. |
| In vivo protocol: | 1. Fiskus W, Sharma S, Shah B, Portier BP, Devaraj SG, Liu K, Iyer SP, Bearss D, Bhalla KN. Highly effective combination of LSD1 (KDM1A) antagonist and pan-histone deacetylase inhibitor against human AML cells. Leukemia. 2014 Nov;28(11):2155-64. doi: 10.1038/leu.2014.119. Epub 2014 Apr 4. Erratum in: Leukemia. 2017 Jul;31(7):1658. PMID: 24699304; PMCID: PMC4739780. |
1: Fiskus W, Sharma S, Shah B, Portier BP, Devaraj SG, Liu K, Iyer SP, Bearss D, Bhalla KN. Highly effective combination of LSD1 (KDM1A) antagonist and pan-histone deacetylase inhibitor against human AML cells. Leukemia. 2014 Nov;28(11):2155-64. doi: 10.1038/leu.2014.119. Epub 2014 Apr 4. PubMed PMID: 24699304.
