2. Protein Tyrosine Kinase/RTK MAPK/ERK Pathway PI3K/Akt/mTOR Apoptosis Epigenetics Cell Cycle/DNA Damage
  3. FGFR p38 MAPK Akt Bcl-2 Family PARP Apoptosis Ferroptosis
  4. FGFR-IN-28

FGFR-IN-28 is a FGFR inhibitor with inhibitory activity against multiple subtypes of the FGFR family, with an IC50 of 4.4 nM against FGFR4. FGFR-IN-28 inhibits kinase activity and phosphorylation processes, and blocks the downstream MAPK and AKT signaling pathways. FGFR-IN-28 induces cellular DNA damage, cell cycle arrest, apoptosis and ferroptosis, and reduces the adhesion, invasion and metastasis abilities of cancer cells. FGFR-IN-28 exhibits anti-tumor activity in in vitro experiments on colon cancer cells, and inhibits tumor growth in colon cancer xenograft models. FGFR-IN-28 can be used in colon cancer-related research.

For research use only. We do not sell to patients.

FGFR-IN-28

FGFR-IN-28 Chemical Structure

CAS No. : 2634677-16-8

Size Stock
50 mg   Get quote  
100 mg   Get quote  
250 mg   Get quote  

* Please select Quantity before adding items.

This product is a controlled substance and not for sale in your territory.

FGFR-IN-28 Related Antibodies

Top Publications Citing Use of Products

View All p38 MAPK Isoform Specific Products:

View All Isoforms
p38 MAPK Akt1 p38α p38β MAPK13 p38δ p38γ

View All Akt Isoform Specific Products:

View All Isoforms
Akt Akt1 Akt2 Akt3

View All Bcl-2 Family Isoform Specific Products:

View All Isoforms
Bcl-2 Bcl-xL Bcl-W Mcl-1 Bfl-1 Bcl-B Bax Bak Bim BNIP3 Bad

View All PARP Isoform Specific Products:

View All Isoforms
PARP PARP1 PARP2 PARP3 PARP4 TNKS1/PARP5A TNKS2/PARP5B PARP7 PARP10 PARP14 PARP15 PARP12 PARP16

  • Biological Activity

  • Purity & Documentation

  • References

  • Customer Review

Description

FGFR-IN-28 is a FGFR inhibitor with inhibitory activity against multiple subtypes of the FGFR family, with an IC50 of 4.4 nM against FGFR4. FGFR-IN-28 inhibits kinase activity and phosphorylation processes, and blocks the downstream MAPK and AKT signaling pathways. FGFR-IN-28 induces cellular DNA damage, cell cycle arrest, apoptosis and ferroptosis, and reduces the adhesion, invasion and metastasis abilities of cancer cells. FGFR-IN-28 exhibits anti-tumor activity in in vitro experiments on colon cancer cells, and inhibits tumor growth in colon cancer xenograft models. FGFR-IN-28 can be used in colon cancer-related research[1].

IC50 & Target[1]

FGFR1

10 nM (IC50)

FGFR2

21 nM (IC50)

FGFR3

50 nM (IC50)

FGFR4

4.4 nM (IC50)

Akt

 

p38 MAPK

 

Bax

 

Bcl-2

 

PARP

 

In Vitro

FGFR-IN-28 (F1-7) dose-dependently inhibits the kinase activity of recombinant FGFR1, FGFR2, FGFR3, and FGFR4 proteins with IC50 values of 10, 21, 50, and 4.4 nmol/L, respectively[1].
FGFR-IN-28 (48 h) dose-dependently reduces the viability of HCT-116, RKO, and SW620 human colon cancer cells with IC50 values of 1.271 μM, 2.046 μM, and 1.433 μM[1].
FGFR-IN-28 (1.0-4.0 μM; 24 h) dose-dependently inhibits the phosphorylation of FGFR, AKT, and MAPK in HCT-116, RKO, and SW620 human colon cancer cells following 12 h of treatment, without altering total FGFR protein levels[1].
FGFR-IN-28 (2.0 μM; 12 h) alters the transcriptome of HCT-116 human colon cancer cells, significantly enriching genes in the MAPK signaling, apoptosis, and ferroptosis pathways[1].
FGFR-IN-28 (1.0-4.0 μM; 24 h) dose-dependently inhibits colony formation in HCT-116, RKO, and SW620 human colon cancer cells[1].
FGFR-IN-28 (1.0-4.0 μM; 48 h) dose-dependently induces apoptosis in HCT-116, RKO, and SW620 human colon cancer cells[1].
FGFR-IN-28 (1.0-4.0 μM; 24 h) dose-dependently modulates apoptosis-related protein expression in HCT-116, RKO, and SW620 human colon cancer cellst, increasing cleaved-PARP and Bax while decreasing Bcl-2[1].
FGFR-IN-28 (4.0 μM) induces cell death in HCT-116 human colon cancer cells via both apoptosis and ferroptosis after 48 h of treatment, as shown by reduced cell death when co-treated with Z-VAD (HY-164388) or ferrostatin-1 (HY-100579), respectively[1].
FGFR-IN-28 (1.0-4.0 μM; 24 h) dose-dependently increases expression of the DNA damage biomarker γ-H2AX in HCT-116 and RKO human colon cancer cells after 24 h of treatment[1].
FGFR-IN-28 (1.0-4.0 μM; 24 h) dose-dependently induces DNA fragmentation, measured via increased comet tail formation, in HCT-116, RKO, and SW620 human colon cancer cells after 24 h of treatment[1].
FGFR-IN-28 (2.0-4.0 μM; 24 h) dose-dependently reduces DNA synthesis and cell proliferation in HCT-116 human colon cancer cells, as measured by decreased EdU incorporation following 24 h of treatment[1].
FGFR-IN-28 (1.0-4.0 μM; 24 h) dose-dependently induces G2/M cell cycle arrest in HCT-116, RKO, and SW620 human colon cancer cells after 24 h of treatment, accompanied by reduced expression of CyclinB1, MDM2, and CDK1[1].
FGFR-IN-28 (1.0-4.0 μM; pretreatment duration not specified; 1 h adhesion incubation) dose-dependently inhibits the adhesion ability of HCT-116, RKO, and SW620 human colon cancer cells[1].

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

FGFR-IN-28 Related Antibodies

Western Blot Analysis[1]

Cell Line: human colon cancer cell lines HCT-116, RKO, SW620
Concentration: 1, 2, 4 μM
Incubation Time: 24 h
Result: Inhibited FGFR phosphorylation in a dose-dependent manner, while total FGFR protein levels remained unchanged.
Reduced phosphorylation levels of downstream signaling proteins AKT and MAPK.
Increased expression of apoptotic markers cleaved-PARP and Bax.
Decreased expression of anti-apoptotic protein Bcl-2.
Increased expression of the DNA damage biomarker γ-H2AX in a dose-dependent manner in both HCT-116 and RKO cells.
Decreased expression of G2/M phase-associated proteins CyclinB1, MDM2, and CDK1 in a dose-dependent manner in HCT-116 and RKO cells.

Cell Proliferation Assay[1]

Cell Line: human colon cancer cell lines HCT-116, RKO, SW620
Concentration: 1, 2, 4 μM
Incubation Time: 24 h (initial treatment, followed by 7 days of culture in fresh medium)
Result: Reduced colony formation of HCT-116, RKO, and SW620 cells in a dose-dependent manner.
Showed greater efficacy than the positive control AZD4547 (HY-13330) at 4 μM.

Apoptosis Analysis[1]

Cell Line: human colon cancer cell lines HCT-116, RKO, SW620
Concentration: 1, 2, 4 μM
Incubation Time: 48 h
Result: Increased the proportion of apoptotic cells in HCT-116, RKO, and SW620 cell lines.

Cell Proliferation Assay[1]

Cell Line: human colon cancer cell line HCT-116
Concentration: 1, 2, 4 μM
Incubation Time: 24 h
Result: Reduced the number of EdU-positive cells in a dose-dependent manner, indicating decreased DNA synthesis and cell proliferation.

Cell Cycle Analysis[1]

Cell Line: human colon cancer cell lines HCT-116, RKO, SW620
Concentration: 1, 2, 4 μM
Incubation Time: 24 h
Result: Increased the proportion of cells arrested in the G2/M phase.
In Vivo

F1-7 (20-40 mg/kg; i.p.; daily; 14 days) exhibits potent dose-dependent anti-tumour activity in a colon cancer xenograft model, with nearly complete tumour growth inhibition at 40 mg/kg via FGFR pathway inhibition, induction of DNA damage, and promotion of cancer cell apoptosis[1].

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

Animal Model: BALB/c (nu/nu) (female, 4-6 weeks old)[1]
Dosage: 20 mg/kg; 40 mg/kg
Administration: i.p.; daily; 14 days
Result: Reduced tumour volume relative to vehicle control. Slowed tumour growth at 20 mg/kg and nearly arrested tumour growth at 40 mg/kg, with markedly decreased tumour weight across treatment groups.
Inhibited FGFR and MAPK phosphorylation in tumour tissue in a dose-dependent manner.
Modulated the expression of apoptosis-related proteins, induced DNA damage, suppressed cell proliferation and facilitated tumour cell apoptosis.
Molecular Weight

533.79

Formula

C24H19Cl3N4O4
CAS No.
SMILES

O=C(C1=CC(NC(CCl)=O)=CC=C1)NC2=NNC3=C2C=CC(C4=C(Cl)C(OC)=CC(OC)=C4Cl)=C3
Shipping

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
  • No file chosen (Maximum size is: 1024 Kb)
  • If you have published this work, please enter the PubMed ID.
  • Your name will appear on the site.

FGFR-IN-28 Related Classifications

  • Molarity Calculator

  • Dilution Calculator

The molarity calculator equation

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass   Concentration   Volume   Molecular Weight *
= × ×

The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
× = ×
C1   V1   C2   V2
Help & FAQs
  • 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:

FGFR-IN-282634677-16-8FGFRp38 MAPKAktBcl-2 FamilyPARPApoptosisFerroptosisFibroblast growth factor receptorPKBProtein kinase Bpoly ADP ribose polymerase SW620AKT signaling pathwaysMAPK signaling pathwaysRKOFGFR4FGFR1FGFR2colon cancerHCT-116FGFR3Inhibitorinhibitorinhibit

Your Recently Viewed Products:

Inquiry Online

Your information is safe with us. * Required Fields.

Product Name

  

Requested Quantity *

Applicant Name *

 

Salutation

Email Address *

 

Phone Number *

Department

 

Organization Name *

City

State

Country or Region *

      

Remarks

Bulk Inquiry

Inquiry Information

Product Name:
FGFR-IN-28
Cat. No.:
HY-184250
Quantity:
MCE Japan Authorized Agent:

Customer Review

Thank You for Your Feedback!

Request for HNMR Report

Please fill out this form to request the QC report. We will send it to your Email address shortly.

Your information is safe with us. * Required Fields.

Product Name

  

Lot #

Applicant Name *

 

Email Address *

Phone Number

 

Department *

Organization Name *

 

Country or Region *

Remarks

SAFETY DATA SHEET (SDS)

Request for HNMR Report

We have received your request and will respond to you as soon as possible.