Art. -Nr.: HY-111485

Ertabresib

Name: Ertabresib
Brand: MedChemExpress
SKU: HY-111485
Price: 110.00 USD
Availability: InStock
Rating: 5 (1 reviews)

(Synonyms: INCB-057643)

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Ertabresib (INCB-057643) is an orally active BET protein inhibitor. Ertabresib blocks gene transcription by targeting the BET protein family, induces cell cycle arrest and apoptosis by downregulating proto-oncogenes such as c-MYC, and additionally reduces the expression of FOXP3 and PD-L1 to improve the immune microenvironment. It also exerts synergistic effects and overcomes drug resistance when combined with chemotherapy and XPO1 inhibitors. Ertabresib can be used in research related to high-grade B-cell lymphoma with MYC and BCL2 rearrangements, pancreatic cancer, pancreatitis, and metastatic castration-resistant prostate cancer.

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Reinheit: 98.34%
CAS. Nr.: 1820889-23-3
Formel: C₂₀H₂₁N₃O₅S
Molecular Weight:415.46

Speicherung:

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

Ertabresib Chemical Structure

CAS. Nr.: 1820889-23-3

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Biologische Aktivität
- Beschreibung
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
- Clinical Trial
Chemical Information
Lösungsmittel & Löslichkeit
- In Vitro
- In Vivo
Reinheit & Dokumentation
Verweise
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

IC₅₀ & Target^[1]^[3]

BET

FOXP3

Alle Epigenetic Reader Domain Isoform-spezifische Produkte anzeigen :

Alle FOXP Isoform-spezifische Produkte anzeigen :

FOXP3

Cellular Effect

Cell Line	Type	Value	Description	References
ASPC1	IC50	204.9 nM	Inhibition of cell viability against human Aspc-1 pancreatic cancer cells assessed by MTT assay following 72 hours of treatment. Inhibition of cell viability against human Aspc-1 pancreatic cancer cells assessed by MTT assay following 72 hours of treatment.	37899423
PANC-1	IC50	2790 nM	Inhibition of cell viability against human PANC-1 pancreatic cancer cells assessed by MTT assay following 72 hours of treatment. Inhibition of cell viability against human PANC-1 pancreatic cancer cells assessed by MTT assay following 72 hours of treatment.	37899423
CAPAN-1	IC50	1040 nM	Inhibition of cell viability against human CAPAN-1 pancreatic cancer cells assessed by MTT assay following 72 hours of treatment. Inhibition of cell viability against human CAPAN-1 pancreatic cancer cells assessed by MTT assay following 72 hours of treatment.	37899423
DU-145	EC50	5.8 μM	Antiproliferative activity against human DU145 prostate cancer cells assessed via MTT assay after 72 hours of incubation. Antiproliferative activity against human DU145 prostate cancer cells assessed via MTT assay after 72 hours of incubation.	33396954
PC-3	EC50	0.35 μM	Antiproliferative activity against human PC3 prostate cancer cells assessed via MTT assay after 72 hours of incubation. Antiproliferative activity against human PC3 prostate cancer cells assessed via MTT assay after 72 hours of incubation.	33396954
22Rv1	EC50	0.43 μM	Antiproliferative activity against human 22Rv1 prostate cancer cells assessed via MTT assay after 72 hours of incubation. Antiproliferative activity against human 22Rv1 prostate cancer cells assessed via MTT assay after 72 hours of incubation.	33396954
LNCaP	EC50	0.17 μM	Antiproliferative activity against human LNCaP prostate cancer cells assessed via MTT assay after 72 hours of incubation. Antiproliferative activity against human LNCaP prostate cancer cells assessed via MTT assay after 72 hours of incubation.	33396954
VCaP	EC50	0.12 μM	Antiproliferative activity against human VCaP prostate cancer cells assessed via MTT assay after 72 hours of incubation. Antiproliferative activity against human VCaP prostate cancer cells assessed via MTT assay after 72 hours of incubation.	33396954
DU-145	CC₅₀	>5 μM	Cytotoxicity against human DU145 prostate cancer cells assessed via trypan blue staining after 72 hours of incubation. Cytotoxicity against human DU145 prostate cancer cells assessed via trypan blue staining after 72 hours of incubation.	33396954
PC-3	CC₅₀	>5 μM	Cytotoxicity against human PC3 prostate cancer cells assessed via trypan blue staining after 72 hours of incubation. Cytotoxicity against human PC3 prostate cancer cells assessed via trypan blue staining after 72 hours of incubation.	33396954
22Rv1	CC₅₀	>5 μM	Cytotoxicity against human 22Rv1 prostate cancer cells assessed via trypan blue staining after 72 hours of incubation. Cytotoxicity against human 22Rv1 prostate cancer cells assessed via trypan blue staining after 72 hours of incubation.	33396954
LNCaP	CC₅₀	>5 μM	Cytotoxicity against human LNCaP prostate cancer cells assessed via trypan blue staining after 72 hours of incubation. Cytotoxicity against human LNCaP prostate cancer cells assessed via trypan blue staining after 72 hours of incubation.	33396954
VCaP	CC₅₀	>5 μM	Cytotoxicity against human VCaP prostate cancer cells assessed via trypan blue staining after 72 hours of incubation. Cytotoxicity against human VCaP prostate cancer cells assessed via trypan blue staining after 72 hours of incubation.	33396954
DU-145	EC50	0.53 μM	Inhibition of colony-forming capability against human DU145 prostate cancer cells assessed via clonogenic assay. Inhibition of colony-forming capability against human DU145 prostate cancer cells assessed via clonogenic assay.	33396954
PC-3	EC50	0.53 μM	Inhibition of colony-forming capability against human PC3 prostate cancer cells assessed via clonogenic assay. Inhibition of colony-forming capability against human PC3 prostate cancer cells assessed via clonogenic assay.	33396954
22Rv1	EC50	0.08 μM	Inhibition of colony-forming capability against human 22Rv1 prostate cancer cells assessed via clonogenic assay. Inhibition of colony-forming capability against human 22Rv1 prostate cancer cells assessed via clonogenic assay.	33396954
LNCaP	EC50	0.09 μM	Inhibition of colony-forming capability against human LNCaP prostate cancer cells assessed via clonogenic assay. Inhibition of colony-forming capability against human LNCaP prostate cancer cells assessed via clonogenic assay.	33396954
VCaP	EC50	0.03 μM	Inhibition of colony-forming capability against human VCaP prostate cancer cells assessed via clonogenic assay. Inhibition of colony-forming capability against human VCaP prostate cancer cells assessed via clonogenic assay.	33396954
DU-145	EC50	3.04 μM	Inhibition of sphere-forming capability against human DU145 prostate cancer cells assessed via prostato-sphere-forming assay. Inhibition of sphere-forming capability against human DU145 prostate cancer cells assessed via prostato-sphere-forming assay.	33396954
PC-3	EC50	0.72 μM	Inhibition of sphere-forming capability against human PC3 prostate cancer cells assessed via prostato-sphere-forming assay. Inhibition of sphere-forming capability against human PC3 prostate cancer cells assessed via prostato-sphere-forming assay.	33396954
22Rv1	EC50	0.20 μM	Inhibition of sphere-forming capability against human 22Rv1 prostate cancer cells assessed via prostato-sphere-forming assay. Inhibition of sphere-forming capability against human 22Rv1 prostate cancer cells assessed via prostato-sphere-forming assay.	33396954
LNCaP	EC50	0.18 μM	Inhibition of sphere-forming capability against human LNCaP prostate cancer cells assessed via prostato-sphere-forming assay. Inhibition of sphere-forming capability against human LNCaP prostate cancer cells assessed via prostato-sphere-forming assay.	33396954
VCaP	EC50	0.17 μM	Inhibition of sphere-forming capability against human VCaP prostate cancer cells assessed via prostato-sphere-forming assay. Inhibition of sphere-forming capability against human VCaP prostate cancer cells assessed via prostato-sphere-forming assay.	33396954

In Vitro

Ertabresib (INCB-057643) (0.01-5.0 µM; 72 h) exerts a significant cell proliferation-inhibiting effect in prostate cancer cell lines (DU145, PC3, 22Rv1, LNCaP, VCaP) and exhibits low cytotoxicity^[1].
Ertabresib (1 nM-25 µM; 7-12 days) potently inhibits colony formation and prostate sphere formation in prostate cancer cell lines^[1].
Ertabresib (72 h) exerts synergistic or additive effects on inhibiting cell growth in prostate cancer cell lines when combined with Docetaxel (HY-B0011), Olaparib (HY-10162), or Carboplatin (HY-17393)^[1].
Ertabresib (500 nM; washed out after 72 h pretreatment) induces complete recovery of cell growth in 22Rv1 cells, but combined treatment with Docetaxe results in more sustained growth inhibition and reduced clonogenicity^[1].
Ertabresib (1 mM for TMD8; 2.5 mM for OCI-LY19; 24 h) exerts a synergistic effect with Selinexor to downregulate the mRNA and protein expression levels of c-Myc in HGBCL-DH cell lines^[2].
Ertabresib (in combination with Selinexor) induces DNA damage and downregulates the phosphorylation level of DNA damage repair kinases in TP53-mutant TMD8 cells, while it upregulates the expression levels of p53 and its downstream targets in TP53-wild-type OCI-LY19 cells ^[2].
Ertabresib inhibits cell proliferation in pancreatic cancer cell lines (Aspc-1, PANC-1, CAPAN-1, Panc1342, PanAsc 2159) following 72 h treatment^[3].
Ertabresib (250 nM-10 mM; 24 h) increases p27^KIP1 protein expression in pancreatic cancer cells (Aspc-1, PanAsc 2159)^[3].
Ertabresib (500 nM-1 mM; 24 h-72 h) downregulates PD-L1 protein and mRNA expression in tumor-conditioned medium-stimulated mouse macrophage cell line RAW 264.7 and pancreatic cancer cells (Aspc-1, PanAsc 2159)^[3].
Ertabresib (100 nM; 4 days) significantly reduces FOXP3 mRNA expression levels in in vitro-activated mouse primary CD4 T cells^[3].
Ertabresib (72 h) induces G1/G0 cell cycle arrest and reduces the proportion of cells in S/G2 phase in DU145, 22Rv1, and LNCaP cells^[1].
Combination of Ertabresib (72 h) with XPO1 inhibitors (Selinexor (HY-17536) or Eltanexor (HY-100423)) exerts synergistic effects in reducing cell viability and promoting apoptosis across multiple HGBCL-DH cell lines with or without TP53 mutations, such as FN, HF, TMD8, VAL, Toledo, OCI-LY19, EJ, Pfeiffer and WILL2^[2].

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

Cell Viability Assay^[2]

Cell Line:

TP53-mutated (FN, HF, TMD8, VAL, Toledo) and TP53 wild-type (OCI-LY19, EJ, Pfeiffer, WILL2) HGBCL-DH cells
Concentration:

15.6 nM, 31.25 nM, 62.5 nM, 125 nM, 250 nM, 500 nM, 1 mM, 2 mM, 2.5 mM, 5 mM, 10 mM
Incubation Time:

72 h
Result:

Decreased cell viability in all tested cell lines in a dose-dependent manner and produced a significant synergistic inhibitory effect when combined with XPO1 inhibitors.

Apoptosis Analysis^[2]

Cell Line:

TP53-mutated (VAL, TMD8, Toledo) and TP53 wild-type (OCI-LY19, EJ, Pfeiffer, WILL2) HGBCL-DH cells, along with MCA cells
Concentration:

500 nM, 625 nM, 1 mM, 1.25 mM, 2 mM, 2.5 mM, 5 mM, 10 mM
Incubation Time:

72 h
Result:

Induced cell apoptosis as a monotherapy, and synergistically increased the proportion of early and late apoptotic cells when combined with XPO1 inhibitors (Selinexor or Eltanexor).

Real Time qPCR^[2]

Cell Line:

TMD8 and OCI-LY19 cells
Concentration:

1 mM (for TMD8), 2.5 mM (for OCI-LY19)
Incubation Time:

24 h
Result:

Significantly downregulated the mRNA transcriptional levels of the MYC gene in cells, with the combination treatment showing a stronger inhibitory effect than monotherapy.

Real Time qPCR^[3]

Cell Line:

mouse macrophage cell line RAW 264.7, primary murine CD4 T cells, pancreatic cancer cell lines
Concentration:

100 nM, 500 nM, 1mM
Incubation Time:

24 h, 72 h or 4 days
Result:

Reduced the mRNA and protein surface expression of PD-L1 in RAW 264.7 macrophages and pancreatic cancer cells; and significantly reduced FOXP3 mRNA expression in in vitro polarized CD4 T cells, indicating its potential to reverse the immunosuppressive microenvironment.

Western Blot Analysis^[3]

Cell Line:

Aspc-1 and PanAsc 2159
Concentration:

250 nM, 1 mM, 2 mM
Incubation Time:

24 h
Result:

Increased the expression of the cell cycle regulator protein p27, indicating the induction of cell cycle arrest.

In Vivo

Ertabresib (INCB-057643) (3 mg/kg or 10 mg/kg; p.o.; 3 mg/kg twice daily, 7 days a week / 10 mg/kg once daily, 5 days a week; treatment duration of 16 days or longer) significantly inhibits tumor growth and reduces tumor weight in a male Nude Foxn1 mouse model with subcutaneous xenografts of 22Rv1 cells [1].
Ertabresib (10 mg/kg; p.o.; once daily; 7 days) alleviates pancreatitis, reduces pancreatic weight, decreases infiltrating activated CD4 T cells, and downregulates the expressions of p-STAT3, COX2, and α-SMA, an activation marker of stellate cells, in a caerulein (HY-A0190)-induced acute pancreatitis model in KC mice^[3].
Ertabresib (10 mg/kg; p.o.; once daily; 2 weeks) slows tumor growth, reduces tumor burden, and induces tumor cell apoptosis in a male mouse model bearing subcutaneous xenografts of TMD8 cells (immunodeficient animals pretreated with total body irradiation)^[2].
Ertabresib (10 mg/kg; p.o.; once daily for consecutive 60 days followed by 5 days per week/or 5 days per week for 16 consecutive weeks starting from 4 weeks of age) exerts effects including prolonging survival, reducing the incidence of liver and lung/diaphragm metastases, decreasing the infiltration of total immune cells and CD4 T cells in the pancreas and liver, and downregulating the expression of immunosuppressive molecules FOXP3 and PD-L1 in the tumor microenvironment in a spontaneous pancreatic cancer model with metastasis in KPC transgenic mice^[3].

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

Animal Model:

Nude Foxn1 male mice (4-5 weeks old) were established by injecting 5-10 x 10⁶ 22Rv1 human prostate cancer cells into the right flank^[1]
Dosage:

3 mg/kg; 10 mg/kg
Administration:

p.o.; the 3 mg/kg group was dosed twice daily (7 days a week), and the 10 mg/kg group was dosed once daily (5 days a week); the treatment duration lasted for 16 days up to the experimental endpoint
Result:

Significantly inhibited tumor growth in mice.
Significantly reduced the final tumor weight.

Animal Model:

Male NOD-Prkdc-/- IL2rg-/- (NPI) immunodeficient mice, pretreated with total body irradiation, were subcutaneously injected with 1 × 10⁷ TMD8 cells to establish a TP53-mutant HGBCL-DH xenograft model^[2]
Dosage:

10 mg/kg
Administration:

p.o.; once daily, treated in combination with Selinexor for 2 weeks
Result:

Combined with Selinexor significantly slowed tumor growth and reduced tumor burden more potently than either monotherapy alone, without significant body weight loss or other unacceptable adverse effects.
TUNEL staining confirmed that the combined treatment induced a higher apoptosis rate.

Animal Model:

KPC genetically engineered mouse model (LSL-KrasG12D/+; LSL-Trp53R172H/+; Pdx-1-Cre) that mimics human pancreatic cancer development and metastasis characteristics^[3]
Dosage:

10 mg/kg
Administration:

p.o.; administered daily for 2 months after tumor confirmation by palpation, then 5 days/week for those surviving beyond 2 months; for microenvironment analysis, administered 5 days/week starting from 4 weeks of age for a duration of 16 weeks
Result:

Significantly prolonged the survival of KPC mice bearing mature tumors (average extension of 55 days) and reduced metastatic burden.
Reduced the infiltration of total immune cells and CD4 T cells in the pancreas, and T cells in the liver.
Decreased the expression of FOXP3 and PD-L1, promoting favorable changes in the immune microenvironment.

Animal Model:

KC genetically engineered mouse model (LSL-KrasG12D/+; Pdx-1-Cre) stimulated with caerulein to induce an acute pancreatitis model^[3]
Dosage:

10 mg/kg
Administration:

p.o.; administered daily for 1 week starting the day after caerulein stimulation
Result:

Significantly attenuated pancreatitis, reduced pancreas weight, decreased the infiltration of activated CD4 T cells, and downregulated the expression of inflammation and fibrosis markers such as p-STAT3, COX2, and α-SMA.

Clinical Trial

NCT Number	Sponsor	Condition	Start Date	Phase A549
NCT01329991	Plexxikon\|		2011-05	PHASE1

Chemical Information

CAS. Nr. 1820889-23-3
Appearance Solid
Molecular Weight 415.46
Formel C₂₀H₂₁N₃O₅S
Color White to off-white
SMILES

O=C1C(C)(C)OC2=C(C3=CN(C)C(C4=C3C=CN4)=O)C=C(S(=O)(C)=O)C=C2N1C
Synonyms

INCB-057643
Versand

Room temperature in continental US; may vary elsewhere.

Speicherung

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

Lösungsmittel & Löslichkeit

In Vitro:

DMSO : 62.5 mg/mL (150.44 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

2.4070 mL

12.0349 mL

24.0697 mL

5 mM

0.4814 mL

2.4070 mL

4.8139 mL

10 mM

0.2407 mL

1.2035 mL

2.4070 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.

Molaritätsrechner

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

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

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: ≥ 2.08 mg/mL (5.01 mM); Clear solution

This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 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% (20% SBE-β-CD in Saline)

Solubility: ≥ 2.08 mg/mL (5.01 mM); Clear solution

This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

Protocol 3

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

Solubility: ≥ 2.08 mg/mL (5.01 mM); Clear solution

This protocol yields a clear solution of ≥ 2.08 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 (20.8 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

Reinheit & Dokumentation

Select Batch:

Reinheit: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (312 KB)
SDS (396 KB)
- English - EN (396 KB)
- Français - FR (396 KB)
- Deutsch - DE (396 KB)
- Norwegian - NO (396 KB)
- Español - ES (396 KB)
- Swedish - SV (396 KB)
- Italian - IT (396 KB)
- Korean - KR (396 KB)
- Portuguese - PT (396 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)

Verweise

[1]. Vázquez R, et al. Efficacy of Novel Bromodomain and Extraterminal Inhibitors in Combination with Chemotherapy for Castration-Resistant Prostate Cancer. European urology oncology. 2021 Jun;4(3):437-446.

[2]. Deng M, et al. The synergy of the XPO1 inhibitors combined with the BET inhibitor INCB057643 in high-grade B-cell lymphoma via downregulation of MYC expression. Scientific reports. 2023 Oct 29;13(1):18554.

[3]. Leal AS, et al. The Bromodomain Inhibitor, INCB057643, Targets Both Cancer Cells and the Tumor Microenvironment in Two Preclinical Models of Pancreatic Cancer. Cancers. 2020 Dec 30;13(1):96. [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	2.4070 mL	12.0349 mL	24.0697 mL	60.1743 mL
	5 mM	0.4814 mL	2.4070 mL	4.8139 mL	12.0349 mL
	10 mM	0.2407 mL	1.2035 mL	2.4070 mL	6.0174 mL
	15 mM	0.1605 mL	0.8023 mL	1.6046 mL	4.0116 mL
	20 mM	0.1203 mL	0.6017 mL	1.2035 mL	3.0087 mL
	25 mM	0.0963 mL	0.4814 mL	0.9628 mL	2.4070 mL
	30 mM	0.0802 mL	0.4012 mL	0.8023 mL	2.0058 mL
	40 mM	0.0602 mL	0.3009 mL	0.6017 mL	1.5044 mL
	50 mM	0.0481 mL	0.2407 mL	0.4814 mL	1.2035 mL
	60 mM	0.0401 mL	0.2006 mL	0.4012 mL	1.0029 mL
	80 mM	0.0301 mL	0.1504 mL	0.3009 mL	0.7522 mL
	100 mM	0.0241 mL	0.1203 mL	0.2407 mL	0.6017 mL

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Ertabresib

BMS-986158

Birabresib

Pelabresib

Apabetalone

ABBV-744

BI-7273

NHWD-870

I-BRD9

I-BET151

PFI-1

Molibresib

JQ-1 carboxylic acid

Alle Epigenetic Reader Domain Isoform-spezifische Produkte anzeigen

Alle FOXP Isoform-spezifische Produkte anzeigen

Biologische Aktivität

Chemical Information

Lösungsmittel & Löslichkeit

Reinheit & Dokumentation

Verweise

Help & FAQs

Complete Stock Solution Preparation Table

Bioz

Ertabresib

BMS-986158

Birabresib

Pelabresib

Apabetalone

ABBV-744

BI-7273

NHWD-870

I-BRD9

I-BET151

PFI-1

Molibresib

JQ-1 carboxylic acid

Alle Epigenetic Reader Domain Isoform-spezifische Produkte anzeigen

Alle FOXP Isoform-spezifische Produkte anzeigen

Biologische Aktivität

Chemical Information

Lösungsmittel & Löslichkeit

Reinheit & Dokumentation

Verweise

Help & FAQs

Complete Stock Solution Preparation Table

Ertabresib Related Classifications

HY-111485 Related Classifications

Bioz