Art. -Nr.: HY-168615

MGD-28

Name: MGD-28
Brand: MedChemExpress
SKU: HY-168615
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MGD-28 is an orally effective cereblon-dependent molecular glue degrader that potently degrades CK1α, IKZF1, IKZF2, and IKZF3, with respective DC₅₀ values of 7.8, 3.8, 56.3, and 7.1 nM. MGD-28 also induces the degradation of multiple novel substrate proteins including ZFP91, DTWD1, ZNFX1, MBD1, and MBD3 via a CRBN/Cullin- and proteasome-dependent mechanism. MGD-28 induces cell apoptosis. MGD-28 is used in the research of multiple myeloma, acute myeloid leukemia, diffuse large B-cell lymphoma, and related malignancies.

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Reinheit : 99.73%
CAS. Nr.: 2991818-13-2
Formel: C₃₃H₃₄FN₇O₃
Molecular Weight:595.67

Speicherung:

Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month

MGD-28 Chemical Structure

CAS. Nr.: 2991818-13-2

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Biologische Aktivität
- Beschreibung
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
Lösungsmittel & Löslichkeit
- In Vitro
- In Vivo
Protokoll (4)
Reinheit & Dokumentation
Verweise
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

IC₅₀ & Target

^[1]

IKZF1

3.8 nM (DC₅₀)

IZKF2

56.3 nM (DC₅₀)

IKZF3

7.1 nM (DC₅₀)

CK1α

7.8 nM (DC₅₀)

Alle IKZF Family Isoform-spezifische Produkte anzeigen :

Alle Casein Kinase Isoform-spezifische Produkte anzeigen :

Cellular Effect

Cell Line	Type	Value	Description	References
RPMI-8226	IC50	0.121 μM	Inhibition of cell growth in human multiple myeloma RPMI-8226 cells assessed by CCK-8 cell viability assay after 96 h incubation. Inhibition of cell growth in human multiple myeloma RPMI-8226 cells assessed by CCK-8 cell viability assay after 96 h incubation.	39218923
NCI-H929	IC50	0.0041 μM	Reduced cell viability after 96 h. Reduced cell viability after 96 h.	39218923
OPM-2	IC50	0.0055 μM	Reduced cell viability after 96 h. Reduced cell viability after 96 h.	39218923
U-937	IC50	0.0088 μM	Reduced cell viability after 96 h. Reduced cell viability after 96 h.	39218923
MOLM-13	IC50	0.0087 μM	Reduced cell viability after 96 h. Reduced cell viability after 96 h.	39218923
MV4-11	IC50	0.0058 μM	Reduced cell viability after 96 h. Reduced cell viability after 96 h.	39218923
KG-1	IC50	0.0069 μM	Reduced cell viability after 96 h. Reduced cell viability after 96 h.	39218923
SKM-1	IC50	0.047 μM	Reduced cell viability after 96 h. Reduced cell viability after 96 h.	39218923
OCI-Ly3	IC50	0.216 μM	Reduced cell viability after 96 h. Reduced cell viability after 96 h.	39218923
SU-DHL-4	EC50	0.303 μM	Reduced cell viability after 96 h. Reduced cell viability after 96 h.	39218923
WSUDLCL2	IC50	0.017 μM	Reduced cell viability after 96 h. Reduced cell viability after 96 h.	39218923
TMD8	IC50	0.147 μM	Reduced cell viability after 96 h. Reduced cell viability after 96 h.	39218923
U2932	IC50	0.113 μM	Reduced cell viability after 96 h. Reduced cell viability after 96 h.	39218923

In Vitro

MGD-28 (dose-response; 24 h) degrades CK1α in a dose-dependent manner in HEK293T cells stably expressing CK1α-HiBiT, with a DC₅₀ of 7.8 nM and a D_max of 90.1%^[1].
MGD-28 (1 μM; 0-24 h) reduces CK1α-HiBiT protein in a time-dependent manner, with CK1α decreasing by >80% as early as 4 h and maintaining a profound degradation level at subsequent time points^[1].
MGD-28 (1 nM-10 μM; 24 h) reduces endogenous CK1α in a dose-dependent manner in NCI-H929 and MV-4-11 cells; a significant reduction of CK1α is observed at concentrations of 1-10 nM in NCI-H929, MV-4-11 and WSU-DLCL-2 cells^[1].
MGD-28 (24 h) degrades IKZF1, IKZF2, and IKZF3, with DC₅₀ values of 3.8, 56.3, and 7.1 nM, and D_max values of 94.1%, 83.3%, and 90.7%, respectively ^[1].
MGD-28 (1 μM; 0-24 h) reduces IKZF1, IKZF2 and IKZF3 in a time-dependent manner; after 4 h of incubation, both IKZF1 and IKZF2 are reduced by >60%, and IKZF3 is reduced by >80%^[1].
MGD-28 (1 μM; 24 h) reduces the levels of CK1α, IKZF1, IKZF2, and IKZF3 in NCI-H929 cells; CRBN deficiency, or pre-incubation with MLN4924 (HY-70062) (1 μM), MG132 (HY-13259) (1 μM), or Pomalidomide (10 μM) for 1 h respectively, can prevent the degradation of these substrates^[1].
MGD-28 (1, 10 μM; 4 h) significantly reduces the abundance of multiple proteins in NCI-H929 cells; the log₂ (fold change) values are -1.95 and -3.39 for CK1α, -1.30 and -5.49 for ZFP91, -0.98 and -5.15 for DTWD1, -1.10 and -3.39 for IKZF1, -2.45 and -4.63 for ZNFX1, -0.67 and -1.62 for ZMIZ2, -2.64 and -5.11 for MBD1, -0.75 and -1.03 for MBD3, and -1.33 and -4.30 for MNT; GSPT1, GSPT2, ZNF654, and ZNF276 do not exhibit the same significant downregulation pattern^[1].
MGD-28 (0.1, 1 μM; 24 h) reduces the protein levels of ZFP91 and DTWD1 in NCI-H929 and MV-4-11 cells, while does not induce significant GSPT1 degradation^[1].
MGD-28 (0.1, 1 μM; 24 h) reduces the protein levels of ZNFX1, MBD1, MBD3, ZMIZ2, and MNT in NCI-H929 and MV-4-11 cells in a dose-dependent manner^[1].
The reducing effect of MGD-28 (1 μM; 0-12 h) on ZNFX1, MBD1, MBD3, ZMIZ2, and MNT intensifies with the extension of incubation time^[1].
MGD-28 (1 μM; 24 h) reduces ZMIZ2 mRNA in NCI-H929 cells, but does not reduce the mRNA levels of ZNFX1, MBD1, MBD3, and MNT^[1].
The reduction of ZNFX1, MBD1, MBD3, ZMIZ2, and MNT proteins induced by MGD-28 (1 μM; 24 h) is prevented by CRBN deficiency, as well as by 1 h of pre-incubation with MLN4924 (1 μM), MG132 (1 μM), or Pomalidomide (10 μM)^[1].
MGD-28 (0.1, 1 μM; 2 h) increases the levels of endogenous ZNFX1, MBD1, and MBD3 that co-immunoprecipitate with CRBN, whereas the co-immunoprecipitation of ZMIZ2 with CRBN does not change significantly, and no co-immunoprecipitation of MNT with CRBN is observed^[1].
MGD-28 (24 h) reduces IKZF1, IKZF2, IKZF3, and CK1α in PDC-7, and significant degradation of these four endogenous proteins is observed at 100 nM^[1].
MGD-28 (96 h) inhibits the viability of MM, AML, and DLBCL cells, with IC₅₀ values of 0.121, 0.0041, 0.0055, 0.0088, 0.0087, 0.0058, 0.0069, 0.047, 0.017, 0.216, 0.303, 0.017, 0.147, and 0.113 μM in RPMI-8226, NCI-H929, OPM-2, U937, MOLM-13, MV-4-11, KG-1, Skm-1, MUTZ-1, Ocl-Ly3, SU-DHL-4, WSU-DLCL-2, TMD8, and U2932 cells, respectively^[1].
MGD-28 (10, 100 nM; 3 days) dose-dependently increases the proportion of Annexin V-positive cells in NCI-H929, MV-4-11 and WSU-DLCL-2 cells^[1].
MGD-28 (96 h) potently reduces the viability of wild-type NCI-H929 cells, and this inhibitory effect on cell viability is markedly attenuated following CRBN deletion^[1].
The inhibitory effect of MGD-28 (96 h) on the viability of MV-4-11 cells is significantly attenuated by Pomalidomide (HY-10984) (10 μM), which supports the mechanism of action of MGD-28 related to competition for the CRBN binding site^[1].
MGD-28 (1 μM) reduces wild-type CK1α and increases p53/p21, but does not exert the same CK1α-degrading effect on the degradation-resistant CK1α^G40N mutant; NCI-H929 cells expressing CK1α^G40N show a significantly reduced cell viability inhibition response to MGD-28^[1].
MGD-28 (4 days) inhibits the viability of PDC-1, PDC-3, PDC-5, and PDC-7 cells, with IC₅₀ values of 9.6, 21.2, 48.6, and 123.4 nM, respectively; as the MM stage progresses, the sensitivity of PDCs to MGD-28 gradually decreases, but its activity remains significantly stronger than that of Pomalidomide^[1].
MGD-28 (4 days) exhibits a weak effect on the cell viability of three primary B cell samples derived from MM, with all IC₅₀ values >10 μM^[1].
MGD-28 (4 days) exhibits broad-spectrum inhibitory effects on cell viability across 46 human solid tumor cell lines, including breast cancer and liver cancer cells^[1].
The combination of MGD-28 and I-BRD9 (HY-18975) for 96 h produces a synergistic inhibitory effect on cell viability in NCI-H929 cells, with a HAS mean synergy score of 15.09; the same combination also exerts a synergistic effect in PDC-7, with a HAS synergy score of 11.93^[1].
MGD-28 (1, 10 μM; 3 days) significantly induces Annexin V-positive apoptosis in wild-type NCI-H929 cells, whereas it barely induces apoptosis in CRBN^−/− NCI-H929 cells^[1].
MGD-28 (0.01-10 μM; 3 days) dose-dependently increases the proportion of Annexin V-positive cells in PDC-7, whereas Lenalidomide (HY-A0003) and Pomalidomide (HY-10984) (each at 10 μM) only produce weak effects^[1].
MGD-28 (1 nM-10 μM) increases the protein levels of p53, p21 and MDM2 in NCI-H929 cells in a dose-dependent manner, and elevates the mRNA expression of CDKN1A/p21 and MDM2 ^[1].

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

Western Blot Analysis^[1]

View Protocol

Cell Line:

NCI-H929, MV-4-11, and WSU-DLCL-2 cells
Concentration:

1-10 nM
Incubation Time:

24 h
Result:

Dose-dependently reduced endogenous CK1α.
Produced marked CK1α depletion at concentrations as low as 1-10 nM.

Apoptosis Analysis^[1]

View Protocol

Cell Line:

NCI-H929, MV-4-11, and WSU-DLCL-2 cells
Concentration:

10 nM, 100 nM
Incubation Time:

3 days
Result:

Induced significant dose-dependent apoptosis in NCI-H929, MV-4-11, and WSU-DLCL-2 cells, with higher potency than lenalidomide or pomalidomide.

Apoptosis Analysis^[1]

View Protocol

Cell Line:

NCI-H929 WT; NCI-H929 CRBN^−/−
Concentration:

1 nM, 10 nM
Incubation Time:

3 days
Result:

Markedly increased Annexin V-positive cells in wild-type NCI-H929 cells.
Produced essentially no apoptosis induction in CRBN^−/− NCI-H929 cells.

Western Blot Analysis^[1]

View Protocol

Cell Line:

NCI-H929
Concentration:

1 nM-10 μM
Incubation Time:

24 h
Result:

Dose-dependently increased p53 protein.
Dose-dependently increased p21 protein.
Dose-dependently increased MDM2 protein.

RT-PCR^[1]

View Protocol

Cell Line:

NCI-H929
Concentration:

1 nM-10 μM
Incubation Time:

24 h
Result:

Increased CDKN1A/p21 mRNA expression.
Increased MDM2 mRNA expression.

Western Blot Analysis^[1]

View Protocol

Cell Line:

NCI-H929; MV-4-11
Concentration:

0.1, 1 μM
Incubation Time:

24 h
Result:

Reduced ZFP91 protein.
Reduced DTWD1 protein.
Did not induce appreciable GSPT1 degradation.
Dose-dependently reduced ZNFX1.
Dose-dependently reduced MBD1.
Dose-dependently reduced MBD3.
Dose-dependently reduced ZMIZ2.
Dose-dependently reduced MNT.

Western Blot Analysis^[1]

View Protocol

Cell Line:

NCI-H929; MV-4-11
Concentration:

1 μM
Incubation Time:

0, 1, 2, 4, 8, 12 h
Result:

Produced progressively greater decreases in ZNFX1 with increasing incubation time.
Produced progressively greater decreases in MBD1.
Produced progressively greater decreases in MBD3.
Produced progressively greater decreases in ZMIZ2.
Produced progressively greater decreases in MNT.

Western Blot Analysis^[1]

View Protocol

Cell Line:

NCI-H929; MV-4-11
Concentration:

MGD-28 1 μM; MLN4924 1 μM; MG132 1 μM; Pomalidomide 10 μM
Incubation Time:

Pretreatment 1 h; MGD-28 24 h
Result:

Reduced ZNFX1, MBD1, MBD3, ZMIZ2, and MNT.
CRBN knockout prevented the decreases in NCI-H929 cells.
MLN4924 prevented the decreases.
MG132 prevented the decreases.
Pomalidomide prevented the decreases.

Apoptosis Analysis^[1]

View Protocol

Cell Line:

PDC-7
Concentration:

0.01, 0.1, 1, 10 μM
Incubation Time:

3 days
Result:

Dose-dependently increased Annexin V-positive cells.
Produced substantially greater apoptosis induction than lenalidomide or pomalidomide at 10 μM.

Parmacokinetics

Species	Dose	Route	T_1/2	C₀	AUC_0-t	AUC_0-inf	V_ss	CL	MRT_0-inf	C_max	T_max	F
Rat^[1]	1 mg/kg	i.v.	1.67 h	463.1 ng/mL	411.7 μg·h/mL	415.1 μg·h/mL	10.22 L/kg	5.79 L/h/kg	1.75 h	/	/	/
Rat^[1]	3 mg/kg	p.o.	1.96 h	/	452.7 μg·h/mL	463.0 μg·h/mL	/	/	6.98 h	127.9 ng/mL	0.71 h	36.7 %

In Vivo

MGD-28 (3 mg/kg; p.o.; qd; 18 days) is administered starting when the tumor volume reaches approximately 80 mm³ in a BALB/c nude mouse xenograft model subcutaneously inoculated with 5 × 10⁶ NCI-H929 cells, and achieves 85.5% TGI on day 10; by day 18, the tumor volume is approximately half of that in the Pomalidomide 10 mg/kg group, and it reduces the proportion of Ki67-positive cells as well as the protein levels of IKZF1, IKZF2, IKZF3, and CK1α in tumor tissues^[1].
MGD-28 (10 mg/kg; p.o.; qd; 18 days) reduces tumor volume below the baseline level at the initiation of administration in the NCI-H929 xenograft tumor model, and achieves complete tumor regression on day 18. It also decreases the number of Ki67-positive cells, significantly downregulates the expression of CK1α, IKZF1, IKZF2 and IKZF3 in tumor tissues, and is only accompanied by slight body weight loss^[1].
MGD-28 (3 mg/kg) is co-administered orally with Dexamethasone (HY-14648) (3 mg/kg) daily for 14 days, which achieves 99.2% TGI on day 10 in the NCI-H929 BALB/c nude mouse xenograft tumor model, while the TGI of Dexamethasone administered alone is 43.7%; the antitumor effect of the combination regimen persists until the end of the experiment, further reducing Ki67-positive cells, with no significant body weight loss or other identifiable toxic manifestations observed^[1].
Combined administration of MGD-28 (3 mg/kg; p.o.; qd) and Tazemetostat (HY-13803) (100 mg/kg; p.o.; qd) for 12 days in the NCI-H929 NOD/SCID mouse xenograft tumor model achieves 95.8% TGI, while Tazemetostat administered alone exerts a weak effect on tumor growth. The combination group exhibits reduced final tumor weight, decreased Ki67-positive cells, and only slight fluctuations in body weight^[1].
Co-administration of MGD-28 (3 mg/kg; p.o.; qd) and Bortezomib (HY-10227) (1 mg/kg) for 12 days induces tumor regression in the NCI-H929 NOD/SCID mouse xenograft model, while Bortezomib administered alone yields a TGI of 29.9%; the combination group further reduces the final tumor weight and the number of Ki67-positive cells, with no significant abnormal changes observed in body weight, major organ weights, or the indicators of leukocytes, erythrocytes, hemoglobin, and platelets ^[1].
MGD-28 (3 mg/kg; p.o.; qd; 24 days) achieves a TGI of 71.9% in the NCI-H929^Pom-R NOD/SCID mouse xenograft tumor model; when administered in combination with I-BRD9 (10 mg/kg; p.o.; qd), the TGI increases to 93.6%. The combination group continuously inhibits tumor growth, further reduces Ki67-positive cells, and exhibits only slight fluctuations in body weight throughout the experimental period^[1].

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

Animal Model:

BALB/c nude (6 weeks old, multiple myeloma xenograft via subcutaneous NCI-H929 cell injection)^[1]
Dosage:

3 mg/kg; 10 mg/kg
Administration:

p.o.; daily; 18 days
Result:

Achieved a tumor growth inhibition (TGI%) value of 85.5% after 10 days at 3 mg/kg.
Reduced tumor volume to approximately half that of the pomalidomide (10 mg/kg) group by day 18 at 3 mg/kg.
Induced complete tumor regression with consistent inhibitory effects throughout the 18-day period at 10 mg/kg.
Significantly reduced levels of IKZF1, IKZF2, IKZF3, and CK1α in harvested tumor tissues at both doses.
Reduced the percentage of Ki67-positive tumor cells at both doses.
Caused only slight weight loss, with both doses well tolerated.

Animal Model:

BALB/c nude (6 weeks old, multiple myeloma xenograft via subcutaneous NCI-H929 cell injection)^[1]
Dosage:

3 mg/kg (in combination with Dexamethasone 3 mg/kg)
Administration:

p.o.; daily; 14 days
Result:

Produced a TGI of 99.2% on day 10.
Exceeded the 43.7% TGI produced by dexamethasone alone.
Maintained pronounced tumor-growth suppression throughout administration.
Further reduced Ki67-positive tumor cells.
Produced no discernible body-weight loss.
Produced no other discernible toxicity signs at the administered doses.

Animal Model:

NOD/SCID (6 weeks old, multiple myeloma xenograft via subcutaneous NCI-H929 cell injection)^[1]
Dosage:

MGD-28 3 mg/kg + Tazemetostat 100 mg/kg
Administration:

p.o.; MGD-28 qd; tazemetostat qd; 12 days
Result:

Produced a TGI of 95.8%.
Produced markedly greater tumor-growth inhibition than tazemetostat alone.
Reduced final tumor weight.
Reduced Ki67-positive tumor cells.
Produced only minimal body-weight fluctuations.
Produced no marked changes in major-organ weights or routine blood parameters.

Animal Model:

NOD/SCID (6 weeks old, pomalidomide-resistant multiple myeloma xenograft via subcutaneous NCI-H929Pom−R cell injection)^[1]
Dosage:

3 mg/kg (single agent); 3 mg/kg (in combination with I-BRD9 10 mg/kg)
Administration:

p.o.; daily; 24 days
Result:

Potently inhibited tumor growth with a tumor growth inhibition (TGI%) value of 71.9% as a single agent at 3 mg/kg.
Achieved a tumor growth inhibition (TGI%) value of 93.6% when combined with I-BRD9, with a more profound inhibitory effect than single-agent therapy.
Resulted in a greater reduction in Ki67-positive tumor cells with combination therapy compared with single-agent therapy.
Caused no discernible body weight loss or toxic effects.

Animal Model:

NOD/SCID mice; NCI-H929 xenograft; administration initiated at approximately 80 mm³^[1]
Dosage:

MGD-28 3 mg/kg + Bortezomib 1 mg/kg
Administration:

p.o.; 12 days
Result:

Induced tumor regression.
Produced substantially greater tumor-growth inhibition than bortezomib alone, which produced a TGI of 29.9%.
Reduced final tumor weight.
Reduced Ki67-positive tumor cells.
Produced only minimal body-weight fluctuations.
Produced no marked changes in major-organ weights.
Produced no marked changes in leukocyte, red blood cell, hemoglobin, or platelet measurements.

Chemical Information

CAS. Nr. 2991818-13-2
Appearance Solid
Molecular Weight 595.67
Formel C₃₃H₃₄FN₇O₃
Color White to off-white
SMILES

CN(N(C1C(NC(CC1)=O)=O)C2=O)CC(C2=CC=C3)=C3NCC(C=C4)=CC=C4CN(CC5)CCN5C6=CC(F)=C(C#N)C=C6
Versand

Room temperature in continental US; may vary elsewhere.

Speicherung

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

Lösungsmittel & Löslichkeit

In Vitro:

DMSO : 100 mg/mL (167.88 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

1.6788 mL

8.3939 mL

16.7878 mL

5 mM

0.3358 mL

1.6788 mL

3.3576 mL

10 mM

0.1679 mL

0.8394 mL

1.6788 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, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

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: ≥ 5 mg/mL (8.39 mM); Clear solution

This protocol yields a clear solution of ≥ 5 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (50.0 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: ≥ 5 mg/mL (8.39 mM); Clear solution

This protocol yields a clear solution of ≥ 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 (50.0 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

Protokoll

All Cell Biology Signal Pathway Related

Detection of 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.
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.
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

Reinheit & Dokumentation

Select Batch:

Reinheit: 99.98%

Assay: 99.98%

ee.: 99.98%

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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]. Li P, et al. Novel potent molecular glue degraders against broad range of hematological cancer cell lines via multiple neosubstrates degradation. Journal of hematology & oncology. 2024 Sep 02;17(1):77. [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, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	1.6788 mL	8.3939 mL	16.7878 mL	41.9695 mL
	5 mM	0.3358 mL	1.6788 mL	3.3576 mL	8.3939 mL
	10 mM	0.1679 mL	0.8394 mL	1.6788 mL	4.1970 mL
	15 mM	0.1119 mL	0.5596 mL	1.1192 mL	2.7980 mL
	20 mM	0.0839 mL	0.4197 mL	0.8394 mL	2.0985 mL
	25 mM	0.0672 mL	0.3358 mL	0.6715 mL	1.6788 mL
	30 mM	0.0560 mL	0.2798 mL	0.5596 mL	1.3990 mL
	40 mM	0.0420 mL	0.2098 mL	0.4197 mL	1.0492 mL
	50 mM	0.0336 mL	0.1679 mL	0.3358 mL	0.8394 mL
	60 mM	0.0280 mL	0.1399 mL	0.2798 mL	0.6995 mL
	80 mM	0.0210 mL	0.1049 mL	0.2098 mL	0.5246 mL
	100 mM	0.0168 mL	0.0839 mL	0.1679 mL	0.4197 mL

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MGD-28

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