SX-682 | CAS#1648843-04-2 | Cxcr1/2 inhibitor

MedKoo Cat#: 206806 | Name: SX-682

Description:

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

SX-682 is a potent and selective Cxcr1/2 inhibitor potentially useful for castration-resistant prostate cancer. CXCR1 and CXCR2 chemokine receptors and their ligands (CXCL1/2/3/7/8) play an important role in tumor progression.

Chemical Structure

SX-682

CAS#1648843-04-2

Theoretical Analysis

MedKoo Cat#: 206806

Name: SX-682

CAS#: 1648843-04-2

Chemical Formula: C19H14BF4N3O4S

Exact Mass: 467.0734

Molecular Weight: 467.20

Elemental Analysis: C, 48.85; H, 3.02; B, 2.31; F, 16.27; N, 8.99; O, 13.70; S, 6.86

Price and Availability

Size	Price	Availability
10mg	USD 150.00	Ready to ship
25mg	USD 250.00	Ready to ship
50mg	USD 450.00	Ready to ship
100mg	USD 750.00	Ready to ship
200mg	USD 1,350.00	Ready to ship
500mg	USD 2,650.00	Ready to ship
1g	USD 3,850.00	Ready to ship
2g	USD 6,450.00	Ready to ship

Bulk Inquiry

Buy Now

Add to Cart

Related CAS #

No Data

Synonym

SX-682; SX 682; SX682.

IUPAC/Chemical Name

(2-(((5-((4-fluorophenyl)carbamoyl)pyrimidin-2-yl)thio)methyl)-4-(trifluoromethoxy)phenyl)boronic acid

InChi Key

SDUDZBCEHIZMFZ-UHFFFAOYSA-N

InChi Code

InChI=1S/C19H14BF4N3O4S/c21-13-1-3-14(4-2-13)27-17(28)12-8-25-18(26-9-12)32-10-11-7-15(31-19(22,23)24)5-6-16(11)20(29)30/h1-9,29-30H,10H2,(H,27,28)

SMILES Code

O=C(C1=CN=C(SCC2=CC(OC(F)(F)F)=CC=C2B(O)O)N=C1)NC3=CC=C(F)C=C3

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

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

More Info

Product Data

Product Data

Certificate of Analysis

View CoA: current batch, Lot# C22R05B14

QC Data

View QC data: current batch, Lot# C22R05B14

Safety Data Sheet (SDS)

View Safety Data Sheet (SDS)

Instruction

View handling instruction

Biological target:

SX-682 is a potent allosteric inhibitor of CXCR1 and CXCR2 that can block tumor myeloid-derived suppressor cells (MDSCs) recruitment and enhance T cell activation and antitumor immunity.

In vitro activity:

TBD

In vivo activity:

As SX-682 enhanced tumor infiltration of endogenous T cells in wild-type mice, it was hypothesized that inhibition of tumor PMN-MDSC infiltration could enhance tumor infiltration of adoptively transferred engineered T cells. RAG1-deficient mice bearing MOC1 or LLC tumors engineered to express OVA257–264 (SIINFEKL) were treated with adoptive transfer of ex vivo–expanded OT-I cytotoxic T lymphocytes (CTLs) with or without SX-682. Following SX-682 treatment alone, tumor accumulation of PMN-MDSCs was abrogated in both models. This reduction in PMN-MDSCs in RAG1-deficient mice correlated with enhanced tumor infiltration of adoptively transferred T cells administered 4 days after initiation of SX-682 treatment. To investigate whether this increase in TIL infiltration was biologically relevant, RAG1-deficient mice bearing SIINFEKL-positive MOC1 or LLC tumors were treated with a combination of SX-682 and OT-I adoptive cell transfer. Treatment with SX-682 chow alone induced no tumor growth inhibition, and treatment with OT-I adoptive cell transfer alone induced some degree of growth delay in both models. These data suggested that, in addition to enhancing antitumor efficacy of PD-axis immune checkpoint blockade, abrogation of PMN-MDSC tumor infiltration with SX-682 can enhance the therapeutic efficacy of adoptively transferred T cells. Reference: JCI Insight. 2019 Apr 4;4(7):e126853. https://pubmed.ncbi.nlm.nih.gov/30944253/

	Solvent	mg/mL	mM
Solubility
	DMSO	171.5	367.08

Note: There can be variations in solubility for the same chemical from different vendors or different batches from the same vendor. The following factors can affect the solubility of the same chemical: solvent used for crystallization, residual solvent content, polymorphism, salt versus free form, degree of hydration, solvent temperature. Please use the solubility data as a reference only. Warming and sonication will facilitate dissolving. Still have questions? Please contact our Technical Support scientists.

Preparing Stock Solutions

The following data is based on the product molecular weight 467.20 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

Formulation protocol:

1. Greene S, Robbins Y, Mydlarz WK, Huynh AP, Schmitt NC, Friedman J, Horn LA, Palena C, Schlom J, Maeda DY, Zebala JA, Clavijo PE, Allen C. Inhibition of MDSC Trafficking with SX-682, a CXCR1/2 Inhibitor, Enhances NK-Cell Immunotherapy in Head and Neck Cancer Models. Clin Cancer Res. 2020 Mar 15;26(6):1420-1431. doi: 10.1158/1078-0432.CCR-19-2625. Epub 2019 Dec 17. PMID: 31848188; PMCID: PMC7073293. 2. Sun L, Clavijo PE, Robbins Y, Patel P, Friedman J, Greene S, Das R, Silvin C, Van Waes C, Horn LA, Schlom J, Palena C, Maeda D, Zebala J, Allen CT. Inhibiting myeloid-derived suppressor cell trafficking enhances T cell immunotherapy. JCI Insight. 2019 Apr 4;4(7):e126853. doi: 10.1172/jci.insight.126853. PMID: 30944253; PMCID: PMC6483637.

In vitro protocol:

TBD

In vivo protocol:

1: Liu X, Tang R, Xu J, Tan Z, Liang C, Meng Q, Lei Y, Hua J, Zhang Y, Liu J, Zhang B, Wang W, Yu X, Shi S. CRIP1 fosters MDSC trafficking and resets tumour microenvironment via facilitating NF-κB/p65 nuclear translocation in pancreatic ductal adenocarcinoma. Gut. 2023 Nov 24;72(12):2329-2343. doi: 10.1136/gutjnl-2022-329349. PMID: 37541772; PMCID: PMC10715495. 2: Yang J, Bergdorf K, Yan C, Luo W, Chen SC, Ayers GD, Liu Q, Liu X, Boothby M, Weiss VL, Groves SM, Oleskie AN, Zhang X, Maeda DY, Zebala JA, Quaranta V, Richmond A. CXCR2 expression during melanoma tumorigenesis controls transcriptional programs that facilitate tumor growth. Mol Cancer. 2023 Jun 3;22(1):92. doi: 10.1186/s12943-023-01789-9. PMID: 37270599; PMCID: PMC10239119. 3: Yang J, Bergdorf K, Yan C, Luo W, Chen SC, Ayers D, Liu Q, Liu X, Boothby M, Groves SM, Oleskie AN, Zhang X, Maeda DY, Zebala JA, Quaranta V, Richmond A. CXCR2 expression during melanoma tumorigenesis controls transcriptional programs that facilitate tumor growth. bioRxiv [Preprint]. 2023 Mar 4:2023.02.22.529548. doi: 10.1101/2023.02.22.529548. Update in: Mol Cancer. 2023 Jun 3;22(1):92. doi: 10.1186/s12943-023-01789-9. PMID: 36865260; PMCID: PMC9980137. 4: Yang J, Yan C, Vilgelm AE, Chen SC, Ayers GD, Johnson CA, Richmond A. Targeted Deletion of CXCR2 in Myeloid Cells Alters the Tumor Immune Environment to Improve Antitumor Immunity. Cancer Immunol Res. 2021 Feb;9(2):200-213. doi: 10.1158/2326-6066.CIR-20-0312. Epub 2020 Nov 11. PMID: 33177110; PMCID: PMC7864868. 5: Rapoport BL, Steel HC, Theron AJ, Smit T, Anderson R. Role of the Neutrophil in the Pathogenesis of Advanced Cancer and Impaired Responsiveness to Therapy. Molecules. 2020 Apr 1;25(7):1618. doi: 10.3390/molecules25071618. PMID: 32244751; PMCID: PMC7180559. 6: Kargl J, Zhu X, Zhang H, Yang GHY, Friesen TJ, Shipley M, Maeda DY, Zebala JA, McKay-Fleisch J, Meredith G, Mashadi-Hossein A, Baik C, Pierce RH, Redman MW, Thompson JC, Albelda SM, Bolouri H, Houghton AM. Neutrophil content predicts lymphocyte depletion and anti-PD1 treatment failure in NSCLC. JCI Insight. 2019 Dec 19;4(24):e130850. doi: 10.1172/jci.insight.130850. PMID: 31852845; PMCID: PMC6975266. 7: Greene S, Robbins Y, Mydlarz WK, Huynh AP, Schmitt NC, Friedman J, Horn LA, Palena C, Schlom J, Maeda DY, Zebala JA, Clavijo PE, Allen C. Inhibition of MDSC Trafficking with SX-682, a CXCR1/2 Inhibitor, Enhances NK-Cell Immunotherapy in Head and Neck Cancer Models. Clin Cancer Res. 2020 Mar 15;26(6):1420-1431. doi: 10.1158/1078-0432.CCR-19-2625. Epub 2019 Dec 17. PMID: 31848188; PMCID: PMC7073293. 8: Sun L, Clavijo PE, Robbins Y, Patel P, Friedman J, Greene S, Das R, Silvin C, Van Waes C, Horn LA, Schlom J, Palena C, Maeda D, Zebala J, Allen CT. Inhibiting myeloid-derived suppressor cell trafficking enhances T cell immunotherapy. JCI Insight. 2019 Apr 4;4(7):e126853. doi: 10.1172/jci.insight.126853. PMID: 30944253; PMCID: PMC6483637.