MGD-28
Based on 1 Customer Validation
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.
Nos produits utilisent uniquement pour la recherche. Nous ne vendons pas aux patients.
- Pureté : 99.73%
- CAS No.: 2991818-13-2
- Formule: C33H34FN7O3
- Masse moléculaire:595.67
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Stockage:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Activité biologique
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Chemical Information
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Solvant et solubilité
- Protocole
- Pureté et documentation
- Références
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Help & FAQs
Activité biologique
Description
IC50 & Target
[1]|
IKZF1 3.8 nM (DC50) |
IZKF2 56.3 nM (DC50) |
IKZF3 7.1 nM (DC50) |
CK1α 7.8 nM (DC50) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| RPMI-8226 | IC50 |
0.121 μM
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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.
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39218923 |
| NCI-H929 | IC50 |
0.0041 μM
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Reduced cell viability after 96 h.
Reduced cell viability after 96 h.
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39218923 |
| OPM-2 | IC50 |
0.0055 μM
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Reduced cell viability after 96 h.
Reduced cell viability after 96 h.
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39218923 |
| U-937 | IC50 |
0.0088 μM
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Reduced cell viability after 96 h.
Reduced cell viability after 96 h.
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39218923 |
| MOLM-13 | IC50 |
0.0087 μM
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Reduced cell viability after 96 h.
Reduced cell viability after 96 h.
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39218923 |
| MV4-11 | IC50 |
0.0058 μM
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Reduced cell viability after 96 h.
Reduced cell viability after 96 h.
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39218923 |
| KG-1 | IC50 |
0.0069 μM
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Reduced cell viability after 96 h.
Reduced cell viability after 96 h.
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39218923 |
| SKM-1 | IC50 |
0.047 μM
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Reduced cell viability after 96 h.
Reduced cell viability after 96 h.
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39218923 |
| OCI-Ly3 | IC50 |
0.216 μM
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Reduced cell viability after 96 h.
Reduced cell viability after 96 h.
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39218923 |
| SU-DHL-4 | EC50 |
0.303 μM
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Reduced cell viability after 96 h.
Reduced cell viability after 96 h.
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39218923 |
| WSUDLCL2 | IC50 |
0.017 μM
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Reduced cell viability after 96 h.
Reduced cell viability after 96 h.
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39218923 |
| TMD8 | IC50 |
0.147 μM
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Reduced cell viability after 96 h.
Reduced cell viability after 96 h.
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39218923 |
| U2932 | IC50 |
0.113 μM
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Reduced cell viability after 96 h.
Reduced cell viability after 96 h.
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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 Dmax 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 Dmax 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 CK1αG40N mutant; NCI-H929 cells expressing CK1αG40N 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.
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Cell Line:NCI-H929, MV-4-11, and WSU-DLCL-2 cells
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Concentration:1-10 nM
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Incubation Time:24 h
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Result:Dose-dependently reduced endogenous CK1α.
Produced marked CK1α depletion at concentrations as low as 1-10 nM.
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Cell Line:NCI-H929, MV-4-11, and WSU-DLCL-2 cells
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Concentration:10 nM, 100 nM
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Incubation Time:3 days
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Result:Induced significant dose-dependent apoptosis in NCI-H929, MV-4-11, and WSU-DLCL-2 cells, with higher potency than lenalidomide or pomalidomide.
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Cell Line:NCI-H929 WT; NCI-H929 CRBN−/−
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Concentration:1 nM, 10 nM
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Incubation Time:3 days
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Result:Markedly increased Annexin V-positive cells in wild-type NCI-H929 cells.
Produced essentially no apoptosis induction in CRBN−/− NCI-H929 cells.
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Cell Line:NCI-H929
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Concentration:1 nM-10 μM
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Incubation Time:24 h
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Result:Dose-dependently increased p53 protein.
Dose-dependently increased p21 protein.
Dose-dependently increased MDM2 protein.
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Cell Line:NCI-H929
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Concentration:1 nM-10 μM
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Incubation Time:24 h
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Result:Increased CDKN1A/p21 mRNA expression.
Increased MDM2 mRNA expression.
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Cell Line:NCI-H929; MV-4-11
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Concentration:0.1, 1 μM
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Incubation Time:24 h
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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.
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Cell Line:NCI-H929; MV-4-11
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Concentration:1 μM
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Incubation Time:0, 1, 2, 4, 8, 12 h
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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.
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Cell Line:NCI-H929; MV-4-11
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Concentration:MGD-28 1 μM; MLN4924 1 μM; MG132 1 μM; Pomalidomide 10 μM
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Incubation Time:Pretreatment 1 h; MGD-28 24 h
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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.
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Cell Line:PDC-7
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Concentration:0.01, 0.1, 1, 10 μM
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Incubation Time:3 days
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Result:Dose-dependently increased Annexin V-positive cells.
Produced substantially greater apoptosis induction than lenalidomide or pomalidomide at 10 μM.
Parmacokinetics
In Vivo
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-H929Pom-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.
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Animal Model:BALB/c nude (6 weeks old, multiple myeloma xenograft via subcutaneous NCI-H929 cell injection)[1]
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Dosage:3 mg/kg; 10 mg/kg
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Administration:p.o.; daily; 18 days
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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.
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Animal Model:BALB/c nude (6 weeks old, multiple myeloma xenograft via subcutaneous NCI-H929 cell injection)[1]
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Dosage:3 mg/kg (in combination with Dexamethasone 3 mg/kg)
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Administration:p.o.; daily; 14 days
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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.
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Animal Model:NOD/SCID (6 weeks old, multiple myeloma xenograft via subcutaneous NCI-H929 cell injection)[1]
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Dosage:MGD-28 3 mg/kg + Tazemetostat 100 mg/kg
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Administration:p.o.; MGD-28 qd; tazemetostat qd; 12 days
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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.
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Animal Model:NOD/SCID (6 weeks old, pomalidomide-resistant multiple myeloma xenograft via subcutaneous NCI-H929Pom−R cell injection)[1]
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Dosage:3 mg/kg (single agent); 3 mg/kg (in combination with I-BRD9 10 mg/kg)
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Administration:p.o.; daily; 24 days
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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.
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Animal Model:NOD/SCID mice; NCI-H929 xenograft; administration initiated at approximately 80 mm3[1]
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Dosage:MGD-28 3 mg/kg + Bortezomib 1 mg/kg
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Administration:p.o.; 12 days
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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
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CAS No. 2991818-13-2
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Appearance Solid
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Masse moléculaire 595.67
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Formule C33H34FN7O3
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Color White to off-white
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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
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Solvant et solubilité
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)
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.
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.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- 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.
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.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%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
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL.
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Protocole
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Detection of Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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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.
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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.
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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
Pureté et documentation
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Fiche technique (303 KB)
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SDS (251 KB)
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Instruction de manipulation (2659 KB)
Références
Complete Stock Solution Preparation Table
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.
| 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 |
MGD-28 Related Classifications
HY-168615 Related Classifications
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