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Cat. No.: HY-184502

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DDO-88109

DDO-88109 is a STING inhibitor with a K_d value of 317 nM for hSTING and 0.625 μM for mSTING. DDO-88109 competitively occupies the CDN-binding pocket of STING, thereby maintaining STING in an inactive state. It inhibits cGAS-STING signaling—including STING translocation from the endoplasmic reticulum to the Golgi apparatus, STING oligomerization, and the phosphorylation of IRF3, p65, TBK1, and STING—and attenuates the production of inflammatory cytokines and tissue inflammation in mouse models of TREX1-deficiency-driven autoinflammation and cisplatin (HY-17394)-induced acute kidney injury. DDO-88109 is suitable for research on inflammatory diseases, autoimmune disorders, and acute kidney injury driven by the cGAS-STING pathway.

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CAS No.: 3034295-80-9
화학식: C₂₄H₂₃BrN₂O
분자량:435.36

보관:

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

DDO-88109 Chemical Structure

CAS No.: 3034295-80-9

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Use of MCE Products

Fluorescent Dye

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

Biological Activity
- 제품 설명
- IC₅₀ & Target
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
순도&문서
References
Calculators
Help & FAQs
Classifications
Bioz

Biological Activity

제품 설명

IC₅₀ & Target^[1]

hSTING-CTD^WT

317 nM (Kd)

hSTING-CTD^AQ / hSTING-CTD^HAQ-related

698 nM (Kd)

hSTING-CTD^H232

960 nM (Kd)

mSTING-CTD^WT

625 nM (Kd)

In Vitro

DDO-88109 (62.5–1000 nM; 90 s contact time, 120 s dissociation time) binds to purified hSTING-CTD^WT protein, with a K_d of 317 nM determined by SPR^[1].
DDO-88109 binds to purified human STING dimers at a 2:1 stoichiometric ratio, with a K_d value of 0.97 μM, and the binding interaction is primarily driven by hydrophobic effects^[1].
DDO-88109 binds to the CDN-binding pocket of the purified hSTING-CTD^WT dimer at a 2:1 stoichiometric ratio, keeping the protein in an inactive conformational state^[1].
DDO-88109 (20-100 μM) binds to purified hSTING-CTD^WT, hSTING-CTD^AQ, and hSTING-CTD^H232 variants in a concentration-dependent manner, which is confirmed by increased ΔT_m values^[1].
DDO-88109 (300-1200 nM; 90 s contact time, 120 s dissociation time) exhibits a K_d of 698 nM for binding to purified hSTING-CTD^AQ, and a K_d of 960 nM for binding to purified hSTING-CTD^H232^[1].
[1].
DDO-88109 (compound incubation for 12 h, stimulation for 3 h) inhibits cGAMP-induced activation of the cGAS-STING pathway in THP1-Dual cells, with an IC₅₀ of 1.76 μM^[1].
DDO-88109 binds to and stabilizes the STING protein in THP1 cells^[1].
DDO-88109 concentration-dependently inhibits cGAMP-induced IFNB transcription in THP1 STING-KO cells expressing hSTING^WT, hSTING^HAQ or hSTING^H232^[1].
DDO-88109 (5 μM) inhibits cGAMP-induced IFNB transcription in HEK293T cells expressing hSTING^WT, hSTING^HAQ or hSTING^H232^[1].
DDO-88109 inhibits cGAMP-induced IFNB and CXCL10 transcription in THP1 cells in a concentration-dependent manner^[1].
DDO-88109 (5 μM) potently inhibits IFNB transcription induced by the cGAS-STING pathway in THP1-derived macrophages, and exhibits excellent selectivity toward other innate immune pathways^[1].
DDO-88109 (0.5-5 μM; 12 h compound incubation followed by 2 h stimulation) inhibits cGAMP-induced phosphorylation of IRF3, p65, TBK1 and STING in THP1 cells in a concentration-dependent manner^[1].
DDO-88109 inhibits cGAMP-induced STING oligomerization and IRF3 dimerization in THP1 cells^[1].
DDO-88109 (5 μM) inhibits cGAMP-induced translocation of STING from the endoplasmic reticulum (ER) to the Golgi apparatus in THP1-derived macrophages^[1].
DDO-88109 binds to purified mSTING-CTD^WT protein in a concentration-dependent manner, as evidenced by the increased ΔTm value^[1].
DDO-88109 inhibits DMXAA-induced activation of the cGAS-STING pathway in RAW-Lucia ISG cells, with an IC₅₀ value of 1.85 μM^[1].
DDO-88109 (5 μM, 4 h) binds to and stabilizes the STING protein in RAW264.7 cells^[1].

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

Western Blot Analysis^[1]

Cell Line:

THP1 cells stimulated with cGAMP
Concentration:

0.5, 1, 2.5, 5 μM
Incubation Time:

12 h compound incubation + 2 h stimulation
Result:

Inhibited cGAMP-induced phosphorylation of IRF3, p65, TBK1 and STING in a concentration-dependent manner.

Parmacokinetics

Species	Dose	Route	T_1/2	V_d	Bioavailability	T_max	C_max
Mice^[1]	2 mg/kg	i.v.	3.19 h	33.50 L/kg	/	/	/
Mice^[1]	5 mg/kg	i.p.	2.91 h	/	59.33 %	0.36 h	213.33 ng/mL
Mice^[1]	20 mg/kg	p.o.	2.54 h	/	26.58 %	0.61 h	198.67 ng/mL

In Vivo

DDO-88109 (5-15 mg/kg; i.p.; daily; 3 days) effectively suppresses cGAS-STING pathway-driven inflammatory cytokine secretion in vivo, as evidenced by reduced plasma IFN-β levels in SR-717-stimulated mice^[1].
DDO-88109 (15 mg/kg; i.p.; daily; 28 days) effectively ameliorates systemic autoinflammation in Trex1^−/− mice, including reducing splenomegaly and T cell activation, with a favorable safety profile compared to H151^[1].
DDO-88109 (5-15 mg/kg; i.p.; daily; 3 days) dose-dependently ameliorates Cisplatin (HY-17394)-induced AKI in mice, improving survival, reducing renal inflammation and injury, and inhibiting cGAS-STING-NF-κB pathway activation^[1].

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

Animal Model:

C57BL/6J (male, 6-8 weeks of age, cGAS-STING pathway activation model induced by SR-717 agonist)^[1]
Dosage:

5 mg/kg; 10 mg/kg; 15 mg/kg
Administration:

i.p.; daily; 3 days
Result:

Significantly reduced plasma IFN-β levels in SR-717-stimulated mice, with efficacy comparable to the positive control H151.

Animal Model:

C57BL/6J Trex1−/− (male, 4 weeks of age, TREX1 deficiency-driven autoinflammation model)^[1]
Dosage:

15 mg/kg
Administration:

i.p.; daily; 28 days
Result:

Normalized spleen weight (with a more potent effect than H151).
Significantly reduced the numbers of effector CD69+ CD4+ and CD8+ T cells.
Reduced memory CD44hiCD62Llo CD4+ and CD8+ T cells in spleens of Trex1−/− mice.
Downregulated transcription of inflammation-related genes in cardiac and renal tissues.
No deaths observed in the treatment group (unlike the H151 group, which had 1 death).

Animal Model:

C57BL/6J (male, 6 weeks of age, cisplatin-induced AKI model)^[1]
Dosage:

5 mg/kg; 10 mg/kg; 15 mg/kg
Administration:

i.p.; daily; 3 days
Result:

Improved endpoint survival rate in a dose-dependent manner (16.7% at 5 mg/kg, higher at elevated doses).
Significantly reduced plasma levels of IL-6, creatinine, and blood urea nitrogen.
Ameliorated renal tubular injury (evidenced by H&E staining and reduced tubular injury scores).
Dose-dependently decreased phosphorylated p65 and TBK1 levels in kidney tissues.
Downregulated transcription of pro-inflammatory cytokines (Cxcl10, Il6, Tnfa, Mcp1) in renal tissues.

Chemical Information

CAS No. 3034295-80-9
분자량 435.36
화학식 C₂₄H₂₃BrN₂O
SMILES

BrC1=CC(C(C(OCC2=CC=C(CN3CCCC3)C=C2)=CC=C4)=C4N5)=C5C=C1
선적

Room temperature in continental US; may vary elsewhere.
보관

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

순도&문서

Handling Instructions (2659 KB)

References

[1]. Li H, et al. Rational design of carbazole-based STING inhibitors for treating cGAS-STING pathway-driven inflammatory disorders. Nature communications. 2026 Jun 02. [Content Brief]

Calculators

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Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

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100 mg

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