2. Cell Cycle/DNA Damage Metabolic Enzyme/Protease Stem Cell/Wnt JAK/STAT Signaling Protein Tyrosine Kinase/RTK Immunology/Inflammation
  3. HSP STAT VEGFR MMP PD-1/PD-L1
  4. HSP110-IN-1

HSP110-IN-1 is a HSP110 inhibitor. HSP110-IN-1 binds to HSP110, inhibits the activity of STAT3, and downregulates the expression of downstream genes VEGF, MMP7 and MMP9. HSP110-IN-1 abrogates IL-6-induced epithelial-mesenchymal transition and inhibits the proliferation of colorectal cancer cells. HSP110-IN-1 remodels the tumor microenvironment by inducing a pro-inflammatory phenotype, regulates macrophages, induces PD-L1 expression, and enhances anti-PD-L1 antibody-mediated tumor regression. HSP110-IN-1 can be used in studies related to colorectal cancer.

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HSP110-IN-1

HSP110-IN-1 Chemical Structure

CAS No. : 2991567-27-0

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HSP110-IN-1 Related Antibodies

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Description

HSP110-IN-1 is a HSP110 inhibitor. HSP110-IN-1 binds to HSP110, inhibits the activity of STAT3, and downregulates the expression of downstream genes VEGF, MMP7 and MMP9. HSP110-IN-1 abrogates IL-6-induced epithelial-mesenchymal transition and inhibits the proliferation of colorectal cancer cells. HSP110-IN-1 remodels the tumor microenvironment by inducing a pro-inflammatory phenotype, regulates macrophages, induces PD-L1 expression, and enhances anti-PD-L1 antibody-mediated tumor regression. HSP110-IN-1 can be used in studies related to colorectal cancer[1][2].

IC50 & Target[1]

HSP110

 

STAT3

 

MMP-9

 

MMP-7

 

In Vitro

HSP110-IN-1 (75 μM; 72 h) potently inhibits the viability of HCT116 and SW480 human colorectal cancer cells, with inhibition rates of 72.9% and 81.3%, respectively[1].
HSP110-IN-1 (0-500 μM; 48 h) inhibits the viability of HCT116 and SW480 human colorectal cancer cells in a dose-dependent manner, with IC50 values of 11.59 μM and 6.05 μM, respectively, and is more potent than the reference compound 1 at equivalent concentrations[1].
HSP110-IN-1 (0-10 μM; 24 h) dose-dependently inhibits STAT3 phosphorylation in HCT116 and SW480 human colorectal cancer cells, without affecting total STAT3 or HSP110 levels, and is more potent than the reference compound 1 at equivalent concentrations[1].
HSP110-IN-1 (5-10 μM; 24 h) downregulates the expression of STAT3 target genes MMP7, MMP9, and VEGF in HCT116 and SW480 human colorectal cancer cells, with greater potency than the reference compound 1 at equivalent concentrations[1].
HSP110-IN-1 (5-10 μM; 48 h) inhibits IL-6-induced migration of HCT116 and SW480 human colorectal cancer cells, with greater potency than the reference compound 1 at 10 μM[1].
HSP110-IN-1 (5-10 μM; 24 h) inhibits IL-6-induced invasion of HCT116 and SW480 human colorectal cancer cells, with greater potency than the reference compound 1 at 10 μM[1].
HSP110-IN-1 (5-10 μM; 24 h) attenuates IL-6-induced epithelial-mesenchymal transition in HCT116 and SW480 human colorectal cancer cells, with greater potency than the reference compound 1 at equivalent concentrations[1].
HSP110-IN-1 (40 μM; 96 h) inhibits the growth of human HCT 116 and HT-29 colorectal cancer 3D spheroids co-cultured with PBMCs[2].
HSP110-IN-1 (40 μM; 48 h) polarizes human M2-like macrophages toward a pro-inflammatory M1-like phenotype and enhances pro-inflammatory marker expression in human M1-like macrophages, while upregulating PD-L1 expression in both macrophage subsets[2].
HSP110-IN-1 (40 μM; 48 h) treatment of M2-like macrophages indirectly promotes proliferation and IFN-γ production in co-cultured autologous human CD8+ T lymphocytes, with this effect amplified by anti-PD-1 co-treatment, while having no direct effect on CD8+ T cell proliferation[2].
HSP110-IN-1 (40 μM; 48 h) treatment of human M1-like or M2-like macrophages enables these macrophages to inhibit the growth of co-cultured HT-29 colorectal cancer 3D spheroids, with enhanced inhibition in the presence of autologous activated T lymphocytes[2].

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

HSP110-IN-1 Related Antibodies

Cell Viability Assay[1]

Cell Line: human colorectal cancer HCT116 and SW480 cells
Concentration: 75 μM
Incubation Time: 72 h
Result: Produced the highest inhibition rate against HCT116 and SW480 cells among tested compounds, with an inhibition rate of 72.9% in HCT116 cells and 81.3% in SW480 cells.

Western Blot Analysis[1]

Cell Line: human colorectal cancer HCT116 and SW480 cells
Concentration: 0, 1.25, 2.5, 5 and 10 μM
Incubation Time: 24 h
Result: Reduced phosphorylated STAT3 levels in a dose-dependent manner in both cell lines, without altering total STAT3 or HSP110 expression.
Inhibited STAT3 phosphorylation more significantly than the reference compound 1 at 5 and 10 μM.

Real Time qPCR[1]

Cell Line: human colorectal cancer HCT116 and SW480 cells
Concentration: 5 and 10 μM
Incubation Time: 24 h
Result: Substantially downregulated the expression of STAT3 downstream target genes MMP7, MMP9, and VEGF in both cell lines.
Exhibited more significant inhibitory effect than the reference compound 1 at 10 μM.

Cell Migration Assay [1]

Cell Line: IL-6-stimulated human colorectal cancer HCT116 and SW480 cells
Concentration: 5 and 10 μM (with 6.25 ng/mL IL-6 stimulation)
Incubation Time: 48 h
Result: Suppressed IL-6-induced cell migration in a dose-dependent manner.
Exhibited more potent inhibitory effects on wound closure than the reference compound 1 at 10 μM.

Cell Invasion Assay[1]

Cell Line: IL-6-stimulated human colorectal cancer HCT116 and SW480 cells
Concentration: 5 and 10 μM (with 6.25 ng/mL IL-6 stimulation)
Incubation Time: 24 h
Result: Suppressed IL-6-induced cell invasion in a dose-dependent manner.
Exhibited more potent inhibitory effects on cell invasion than the reference compound 1 at 10 μM.

Western Blot Analysis[1]

Cell Line: IL-6-stimulated human colorectal cancer HCT116 and SW480 cells
Concentration: 5 and 10 μM (with 6.25 ng/mL IL-6 stimulation)
Incubation Time: 24 h
Result: Increased the expression of epithelial marker E-cadherin and decreased the expression of mesenchymal markers N-cadherin and Snail in IL-6-stimulated cells.
Produced more significant reversal of EMT markers than the reference compound 1 at 5 and 10 μM.
Parmacokinetics
Species Dose Route Bioavailability T1/2 Vss CL
Mice[1] 5 mg/kg i.v. / 6.55 h 4.18 L/kg 551.60 mL/h/kg
Mice[1] 10 mg/kg p.o. 4.2 % 5.25 h / /
In Vivo

HSP110-IN-1 (Compound C7) (5 mg/kg; i.p.; every three days; 30 days) exerts significant in vivo tumor growth inhibition in HCT116 xenograft mice, with greater efficacy than the first-generation HSP110 inhibitor, accompanied by reduced VEGF and MMP9 expression and increased p53 expression in tumor tissue relative to both vehicle control and compound 1[1].
HSP110-IN-1 (Compound C7) (5 mg/kg; i.p.; three times weekly; 21 days) induces a 75-80% reduction in CT26 colorectal tumor growth in BALB/c mice, reshapes the tumor microenvironment toward a pro-inflammatory state, and upregulates PD-L1 expression in multiple cell types without detectable toxicity at the tested dose[2].
HSP110-IN-1 (Compound C7) (5 mg/kg; i.p.; three times weekly; 21 days) potentiates the efficacy of anti-PD-L1 therapy in anti-PD-L1-resistant CT26 colorectal tumors in BALB/c mice, enhancing tumor regression, reshaping the tumor microenvironment, and promoting functional CD8+ tumor-infiltrating lymphocytes[2].
HSP110-IN-1 (Compound C7) (5 mg/kg; i.p.; three times weekly; 21 days) enhances the efficacy of anti-PD-L1 therapy in anti-PD-L1-sensitive MC38 colorectal tumors in C57BL/6 mice, driving superior tumor regression and reshaping the tumor microenvironment[2].

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

Animal Model: BALB/c nude mice (male, 4-6 weeks old, 18-23 g, HCT116 human colorectal cancer cell xenograft)[1]
Dosage: 5 mg/kg
Administration: i.p.; every three days; 30 days
Result: Reduced tumor volumes and weights significantly.
Reduced expression of STAT3 downstream genes VEGF and MMP9 significantly in tumor tissues.
Increased expression of tumor suppressor protein p53 significantly in tumor tissues.
Caused no significant changes in body weight.
Animal Model: BALB/c (8-10-week-old female; subcutaneous injection of 5×105 CT26 wild-type cells)[2]
Dosage: 5 mg/kg
Administration: i.p.; three times weekly; 21 days
Result: Induced a 75-80% reduction in tumor growth compared to vehicle controls.
Increased tumor cell apoptosis and reduced phosphorylated STAT3 levels in tumor tissue compared to vehicle and first-generation inhibitor C33.
Reduced the expression of pro-tumoral M2-like tumor-associated macrophage marker CD206 without affecting M1-like marker CD80.
Increased PD-L1 expression in tumor-associated macrophages, tumor cells, myeloid-derived suppressor cells, and dendritic cells.
No toxicity detected via intestinal crypt apoptosis staining or body weight loss.\nSignificantly reduced tumor growth compared to vehicle.
When combined with anti-PD-L1, induced greater tumor regression than either monotherapy, including in the anti-PD-L1-resistant CT26 model.
Decreased CD206 expression in tumor-associated macrophages when used alone or in combination with anti-PD-L1.
Increased PD-L1 expression in tumor cells and M2-like macrophages, which was reduced by co-administration of anti-PD-L1.
Increased the percentage of CD8+ tumor-infiltrating lymphocytes co-expressing PD-1 and TIM-3 or PD-1 and LAG-3, which exhibited enhanced effector function (higher expression of granzyme B, IFN-γ, and IL-2) compared to monotherapies or vehicle.
Animal Model: C57BL/6 (8-10-week-old female; subcutaneous injection of 5×105 MC38 cells)[2]
Dosage: 5 mg/kg
Administration: i.p.; three times weekly; 21 days
Result: Significantly reduced tumor growth compared to vehicle.
When combined with anti-PD-L1, induced greater tumor regression than either monotherapy in the anti-PD-L1-sensitive MC38 model.
Decreased CD206 expression in tumor-associated macrophages when used alone or in combination with anti-PD-L1.
Increased PD-L1 expression in tumor cells and M2-like macrophages, which was reduced by co-administration of anti-PD-L1.
Molecular Weight

516.59

Formula

C29H32N4O5
CAS No.
SMILES

COC1=CC=C(C=C1OC)N2CC3CN(CC3C2)C4=C(C=C(C=N4)C5=CC(OC)=C(C(OC)=C5)OC)C#N
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Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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HSP110-IN-1 Related Classifications

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

HSP110-IN-12991567-27-0HSPSTATVEGFRMMPPD-1/PD-L1Heat shock proteinsVascular endothelial growth factor receptorMatrix metalloproteinasesPD-1/Programmed death-ligand 1colorectal cancerHSP110SW480epithelial-mesenchymal transitionmacrophagesMMP7STAT3VEGFMMP9HCT116Inhibitorinhibitorinhibit

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