Cat. No.: HY-10325

CL-387785

Name: CL-387785
Brand: MedChemExpress
SKU: HY-10325
Price: 60.00 USD
Availability: InStock
Rating: 5 (2 reviews)

(Synonyms: EKI-785; WAY-EKI 785)

2 Cited Publications

Customer Review

Based on 2 publication(s) in Google Scholar

CL-387785 (EKI-785; WAY-EKI 785) is an orally active EGFR inhibitor with an IC₅₀ of 370 pM. CL-387785 inhibits EGF-stimulated EGFR autophosphorylation with an IC₅₀ of approximately 5 nM. CL-387,785 exerts selective inhibition on cell lines overexpressing EGFR or c-erbB-2, whereas it shows weak inhibitory effects on cell lines with low expression of these two receptors. CL-387785 effectively induces cell cycle arrest and apoptosis. CL-387785 can be used for the research of non-small cell lung cancer and autosomal recessive polycystic kidney disease.

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

Purity : 99.31%
CAS No.: 194423-06-8
Formula: C₁₈H₁₃BrN₄O
Molecular Weight:381.23

Storage:

Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 2 years , -20°C, 1 year

CL-387785 Chemical Structure

CAS No.: 194423-06-8

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Antibody-Drug Conjugates

One-stop solution for XDC (ADC/PDC/RDC/ApDC/FDC/ISAC/VDC/SMDC)

Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Publications (2)
Solvent & Solubility
- In Vitro
- In Vivo
Protocols (9)
Purity & Documentation
References
Help & FAQs
Classifications
Bioz

Biological Activity

Description

IC₅₀ & Target

^[1]

EGFR

370 pM (IC₅₀)

All EGFR Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
A-431	IC₅₀	0.079 μM Compound: 1	Inhibition of cell growth of human epidermoid carcinoma xenograft (A431) model using cell based assay Inhibition of cell growth of human epidermoid carcinoma xenograft (A431) model using cell based assay	[PMID: 11495584]
A-431	IC₅₀	5 nM Compound: 14, CL-387785	Inhibition of EGF-induced autophosphorylation of EGFR in human A431 cells Inhibition of EGF-induced autophosphorylation of EGFR in human A431 cells	[PMID: 22621397]
BaF3	IC₅₀	>3.3 μM Compound: CL-387,785	Antiproliferative activity against mouse BaF3 cells harboring EGFR L858R/T790M double mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay Antiproliferative activity against mouse BaF3 cells harboring EGFR L858R/T790M double mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay	[PMID: 20033049]
BaF3	IC₅₀	1.06 μM Compound: CL-387,785	Antiproliferative activity against mouse BaF3 cells harboring EGFR E746_A750/T790M mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay Antiproliferative activity against mouse BaF3 cells harboring EGFR E746_A750/T790M mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay	[PMID: 20033049]
BaF3	IC₅₀	2 nM Compound: CL-387,785	Antiproliferative activity against mouse BaF3 cells harboring EGFR E746_A750 mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay Antiproliferative activity against mouse BaF3 cells harboring EGFR E746_A750 mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay	[PMID: 20033049]
BaF3	IC₅₀	2 nM Compound: CL-387,785	Antiproliferative activity against mouse BaF3 cells harboring EGFR vIII mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay Antiproliferative activity against mouse BaF3 cells harboring EGFR vIII mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay	[PMID: 20033049]
BaF3	IC₅₀	2.69 μM Compound: CL-387,785	Antiproliferative activity against mouse BaF3 cells harboring EGFR L858R/T790M/C797S triple mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay Antiproliferative activity against mouse BaF3 cells harboring EGFR L858R/T790M/C797S triple mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay	[PMID: 20033049]
BaF3	IC₅₀	2.81 μM Compound: CL-387,785	Antiproliferative activity against mouse BaF3 cells harboring EGFR A767_V769dupASV mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay Antiproliferative activity against mouse BaF3 cells harboring EGFR A767_V769dupASV mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay	[PMID: 20033049]
BaF3	IC₅₀	26 nM Compound: CL-387,785	Antiproliferative activity against mouse BaF3 cells harboring wildtype ERBB2 assessed as inhibition of cell growth incubated for 72 hrs by MTS assay Antiproliferative activity against mouse BaF3 cells harboring wildtype ERBB2 assessed as inhibition of cell growth incubated for 72 hrs by MTS assay	[PMID: 20033049]
BaF3	IC₅₀	3.17 μM Compound: CL-387,785	Antiproliferative activity against mouse BaF3 cells harboring EGFR E746_A750/T790M/C797S mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay Antiproliferative activity against mouse BaF3 cells harboring EGFR E746_A750/T790M/C797S mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay	[PMID: 20033049]
BaF3	IC₅₀	4 nM Compound: CL-387,785	Antiproliferative activity against mouse BaF3 cells harboring EGFR L858R mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay Antiproliferative activity against mouse BaF3 cells harboring EGFR L858R mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay	[PMID: 20033049]
BaF3	IC₅₀	75 nM Compound: CL-387,785	Antiproliferative activity against mouse BaF3 cells harboring ERBB2 Ins 774YVMA mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay Antiproliferative activity against mouse BaF3 cells harboring ERBB2 Ins 774YVMA mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay	[PMID: 20033049]
BaF3	IC₅₀	8 nM Compound: CL-387,785	Antiproliferative activity against mouse BaF3 cells harboring ERBB2 Ins G776V,C mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay Antiproliferative activity against mouse BaF3 cells harboring ERBB2 Ins G776V,C mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay	[PMID: 20033049]
Calu-3	IC₅₀	100 nM Compound: CL-387,785	Antiproliferative activity against human Calu-3 cells harboring ERBB2 amp mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay Antiproliferative activity against human Calu-3 cells harboring ERBB2 amp mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay	[PMID: 20033049]
HCC827	IC₅₀	2 nM Compound: CL-387,785	Antiproliferative activity against human HCC827 cells harboring EGFR Del E746_A750 mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay Antiproliferative activity against human HCC827 cells harboring EGFR Del E746_A750 mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay	[PMID: 20033049]
NCI-H1975	IC₅₀	850 nM Compound: CL-387,785	Antiproliferative activity against human NCI-H1975 cells harboring EGFR L858R/T790M mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay Antiproliferative activity against human NCI-H1975 cells harboring EGFR L858R/T790M mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay	[PMID: 20033049]
NCI-H3255	IC₅₀	23 nM Compound: CL-387,785	Antiproliferative activity against human NCI-H3255 cells harboring EGFR L858R mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay Antiproliferative activity against human NCI-H3255 cells harboring EGFR L858R mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay	[PMID: 20033049]
NIH3T3	IC₅₀	2.5 nM Compound: 20	Inhibition of EGF stimulated human erbB1 autophosphorylation in NIH3T3 cells Inhibition of EGF stimulated human erbB1 autophosphorylation in NIH3T3 cells	[PMID: 16480284]
PC-9	IC₅₀	2 nM Compound: CL-387,785	Antiproliferative activity against human PC-9 cells harboring EGFR Del E746_A750 mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay Antiproliferative activity against human PC-9 cells harboring EGFR Del E746_A750 mutant assessed as inhibition of cell growth incubated for 72 hrs by MTS assay	[PMID: 20033049]
Sf9	IC₅₀	0.2 μM Compound: EKI-785	TP_TRANSPORTER: efflux of Hoechst33342 in BCRP-expressing Sf9 cells TP_TRANSPORTER: efflux of Hoechst33342 in BCRP-expressing Sf9 cells	[PMID: 15155841]
SK-BR-3	IC₅₀	0.017 μM Compound: 1	Inhibition of cell growth of SKBr3 cell lines using cell-based assay Inhibition of cell growth of SKBr3 cell lines using cell-based assay	[PMID: 11495584]
SW-620	IC₅₀	1.5 μM Compound: 1	Inhibition of cell growth of SW620 cell lines using cell-based assay Inhibition of cell growth of SW620 cell lines using cell-based assay	[PMID: 11495584]

In Vitro

CL-387,785 (30-1000 nM; 3 days) induces G0/G1 cell cycle arrest in A431 and SK-BR-3 cells at concentrations of 300-1000 nM after 3 days of incubation, with minimal apoptosis at higher doses^[2].
CL-387,785 (0.1-30 μM; 48 h) inhibits the growth of gefitinib-resistant Ba/F3-EGFR^L858R-T790M cells with a cellular IC₅₀ of ~1 μmol/L^[3].
CL-387,785 (3 μM; 24 h) induces significant apoptosis in gefitinib-resistant Ba/F3-EGFR^L858R-T790M cells and sensitive Ba/F3-EGFR^L858R cells^[3].
CL-387,785 (0.3-10 μM; 6 h) inhibits phosphorylation of EGFR and its downstream signaling targets STAT5, AKT, and ERK 1/2 in gefitinib-resistant Ba/F3-EGFR^L858R-T790M cells with an IC₅₀ of ~1 μmol/L^[3].
CL-387,785 (0.1-3 μM; 6 h) completely inhibits phosphorylation of EGFR and its downstream signaling targets STAT5, AKT, and ERK 1/2 in gefitinib-resistant H1975 lung cancer cells^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.

Cell Cycle Analysis^[2]

View Protocol

Cell Line:

A431 cells; SK-BR-3 cells
Concentration:

30, 300, 1000 nM
Incubation Time:

3 days
Result:

Increased the percentage of A431 cells in G0/G1 phase to 73% from 56% in untreated controls, with corresponding decreases in S phase (16% vs 28%) and G2/M phase (8% vs 15%) at 300 nM.
Increased SK-BR-3 cells in G0/G1 phase to 82% and 84%, respectively, from 63% in controls, with S phase reduced to 4% and 4%, and G2/M phase reduced to 3% and 3% at 300 nM and 1000 nM.
Induced 7% apoptotic cells in A431 cells at 1000 nM, and 10-11% apoptotic cells in SK-BR-3 cells at 300-1000 nM.

Apoptosis Analysis^[3]

View Protocol

Cell Line:

Ba/F3-L858R, Ba/F3-L858R-T790M stable cell lines
Concentration:

3 μM
Incubation Time:

24 h
Result:

Induced high levels of apoptosis in both Ba/F3-L858R and gefitinib-resistant Ba/F3-L858R-T790M cells, with apoptosis rates comparable to those induced by gefitinib in Ba/F3-L858R cells.

Western Blot Analysis^[3]

View Protocol

Cell Line:

Ba/F3-L858R, Ba/F3-L858R-T790M stable cell lines
Concentration:

0.3, 1, 3 and 10 μM
Incubation Time:

6 h
Result:

Potently inhibited phosphorylation of EGFR, STAT5, AKT, and ERK 1/2 in both Ba/F3-L858R and gefitinib-resistant Ba/F3-L858R-T790M cells, with an IC₅₀ of ~1 μM for inhibition of all examined phosphorylated proteins in Ba/F3-L858R-T790M cells.

Apoptosis Analysis^[3]

View Protocol

Cell Line:

H1975 (lung adenocarcinoma, EGFR L858R-T790M mutant) cell line
Concentration:

1 μM
Incubation Time:

48 h
Result:

Induced a mean apoptotic cell percentage of 42.1% in H1975 cells, a statistically significant increase compared to control (8.84%) and gefitinib-treated (8.73%) cells.

Western Blot Analysis^[3]

View Protocol

Cell Line:

H1975 (lung adenocarcinoma, EGFR L858R-T790M mutant) cell line
Concentration:

0.3, 1, 3 and 10 μM
Incubation Time:

6 h
Result:

Completely inhibited phosphorylation of EGFR, STAT5, AKT, and ERK 1/2 in H1975 cells at 1 μM.

In Vivo

CL-387785 (25-100 mg/kg; intraperitoneal injection; once every 3 days; days 18-46) dose-dependently reduces collecting duct cyst formation, improves renal function, attenuates biliary abnormalities, and prolongs survival in autosomal recessive polycystic kidney disease mice^[1].
CL-387785 (20-80 mg/kg; i.p., p.o.; intermittent administration with repeated dosing for 10 consecutive days) inhibits the growth of EGF-R-overexpressing A431 tumors in nude mice, and the tumors respond to the repeated dosing regimen^[2].

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

Animal Model:

Balb/c-bpk/bpk (postnatal)^[1]
Dosage:

25 mg/kg; 50 mg/kg; 60 mg/kg; 80 mg/kg; 90 mg/kg (short-term and long-term survival studies); 100 mg/kg
Administration:

i.p.; every 3 days; 6 total doses (short-term); every 3 days from postnatal day 7 to postnatal day 46 (long-term survival)
Result:

Effectively alleviated the cyst growth and bile duct lesions in the ARPKD model mice, improved renal function, and significantly prolonged their lifespan.

Animal Model:

Athymic nu/nu (female)^[2]
Dosage:

80 mg/kg (i.p., intermittent schedule); 20 mg/kg (i.p., daily x10 days, repeated); 80 mg/kg (p.o., daily x10 days, repeated)
Administration:

i.p. (days 1, 5, 9, 21, 25, 29); i.p. (daily on days 1 through 10 and days 21 through 30); p.o. (daily on days 1 through 10 and days 21 through 30)
Result:

Produced significant tumor growth inhibition.
Showed tumor regrowth after initial 10-day treatment course, but tumors responded to a second 10-day treatment course.

Chemical Information

CAS No. 194423-06-8
Appearance Solid
Molecular Weight 381.23
Formula C₁₈H₁₃BrN₄O
Color Light yellow to yellow
SMILES

O=C(NC1=CC2=C(NC3=CC=CC(Br)=C3)N=CN=C2C=C1)C#CC
Synonyms

EKI-785; WAY-EKI 785
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	2 years
	-20°C	1 year

Publications (2)

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Journal Impact Factor

Int J Biol Sci

Targeted Induction of Cancer Cell Necroptosis Potentiates Anti-PD-1 Immunotherapy via CD80 Activation. [Abstract]

2026 Jan 22;22(4):2085-2100. PMID: 41694588
Int J Oncol

Exosomes from PYCR1 knockdown bone marrow mesenchymal stem inhibits aerobic glycolysis and the growth of bladder cancer cells via regulation of the EGFR/PI3K/AKT pathway. [Abstract]

2023 Jul 9;63(1):84. PMID: 37293856

Solvent & Solubility

In Vitro:

DMSO : 100 mg/mL (262.31 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

2.6231 mL

13.1154 mL

26.2309 mL

5 mM

0.5246 mL

2.6231 mL

5.2462 mL

10 mM

0.2623 mL

1.3115 mL

2.6231 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.

Molarity Calculator

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

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Dilution Calculator

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In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline

Solubility: ≥ 2.5 mg/mL (6.56 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

Protocol 2

Add each solvent one by one: 10% DMSO 90% Corn Oil

Solubility: ≥ 2.5 mg/mL (6.56 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

Dosage Dosage
mg/kg
Animal Weight (Per Animal) Animal Weight (Per Animal)
g
Dosing Volume (Per Animal) Dosing Volume (Per Animal)
μL
Number of Animals Number of Animals

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Please enter your animal formula composition:

%
DMSO +

Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
%
+
+
%
Tween-80 + +
%
Saline +

The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).

Working solution concentration: 0.22 mg/mL

Protocols

All Molecular Biology Cell Biology Signal Pathway Related

RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
Flow cytometric DNA-content cell-cycle staining
Flow cytometric DNA-content cell-cycle staining measures the fluorescence intensity of DNA-bound fluorochromes in single cells or nuclei to estimate DNA content distributions, allowing assignment of populations to G0/G1, S, and G2/M phases by DNA histogram deconvolution. Propidium iodide (PI) intercalates into DNA, and PI fluorescence is proportional to cellular DNA content when staining is performed under conditions that make DNA accessible and minimize non-DNA signal. Cells with G2/M DNA content are expected to show approximately twice the fluorescence intensity of G0/G1 cells, while S-phase cells occupy intermediate fluorescence values. PI-based DNA-content analysis can also detect cells with fractional DNA content, often reported as sub-G1, when DNA fragmentation and extraction during staining reduce retained DNA signal in apoptotic cells. DAPI is an alternative DNA fluorochrome for univariate DNA-content analysis, while bivariate approaches combining DNA content with proliferation
Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
BrdU Incorporation Assay
Bromodeoxyuridine (BrdU) incorporation assay is based on the principle that BrdU, a thymidine analog, is incorporated into newly synthesized DNA during the S phase of the cell cycle, thereby serving as a marker of DNA replication and cellular proliferation. Incorporated BrdU can be detected using anti-BrdU antibodies following DNA denaturation, enabling visualization or quantification of proliferating cells through immunochemical detection methods such as immunofluorescence or immunohistochemistry.
Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
Protocol for Cell Cycle
Cell-cycle analysis by flow cytometry measures DNA content in single cells to estimate the fraction of cells in G0/G1, S, and G2/M phases. Propidium iodide intercalates into DNA, and after RNA removal with RNase, fluorescence intensity reflects cellular DNA content: 2N cells are assigned to G0/G1, cells between 2N and 4N to S phase, and 4N cells to G2/M. DNA-content analysis alone cannot reliably separate G0 from G1 or G2 from M. Ki-67 can distinguish quiescent G0 cells from cycling cells, EdU or BrdU incorporation marks active DNA synthesis in S phase, and phospho-histone H3 staining identifies mitotic cells within the 4N population.

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (291 KB)
SDS (644 KB)
- English - EN (644 KB)
- Français - FR (644 KB)
- Deutsch - DE (644 KB)
- Norwegian - NO (644 KB)
- Español - ES (644 KB)
- Swedish - SV (644 KB)
- Italian - IT (644 KB)
- Korean - KR (644 KB)
- Portuguese - PT (644 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[1]. Sweeney WE, et al. Treatment of polycystic kidney disease with a novel tyrosine kinase inhibitor. Kidney Int. 2000 Jan;57(1):33-40.
[Content Brief]

[2]. Discafani CM, et al. Irreversible inhibition of epidermal growth factor receptor tyrosine kinase with in vivo activity by N-[4-[(3-bromophenyl)amino]-6-quinazolinyl]-2-butynamide (CL-387,785). Biochem Pharmacol. 1999;57(8):917-925. [Content Brief]

[3]. Kobayashi S, et al. An alternative inhibitor overcomes resistance caused by a mutation of the epidermal growth factor receptor. Cancer Res. 2005 Aug 15;65(16):7096-101.
[Content Brief]

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.

Complete Stock Solution Preparation Table

Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	2.6231 mL	13.1154 mL	26.2309 mL	65.5772 mL
	5 mM	0.5246 mL	2.6231 mL	5.2462 mL	13.1154 mL
	10 mM	0.2623 mL	1.3115 mL	2.6231 mL	6.5577 mL
	15 mM	0.1749 mL	0.8744 mL	1.7487 mL	4.3718 mL
	20 mM	0.1312 mL	0.6558 mL	1.3115 mL	3.2789 mL
	25 mM	0.1049 mL	0.5246 mL	1.0492 mL	2.6231 mL
	30 mM	0.0874 mL	0.4372 mL	0.8744 mL	2.1859 mL
	40 mM	0.0656 mL	0.3279 mL	0.6558 mL	1.6394 mL
	50 mM	0.0525 mL	0.2623 mL	0.5246 mL	1.3115 mL
	60 mM	0.0437 mL	0.2186 mL	0.4372 mL	1.0930 mL
	80 mM	0.0328 mL	0.1639 mL	0.3279 mL	0.8197 mL
	100 mM	0.0262 mL	0.1312 mL	0.2623 mL	0.6558 mL

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CL-387785

Publications Citing Use of MedChemExpress (MCE) CL-387785

All EGFR Isoforms