Cat. No.: HY-148837

GT19630

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GT19630 is an orally active c-Myc PROTAC targeted degrader based on the cereblon E3 ubiquitin ligase, with an IC₅₀ of 1.5 nM against human c-Myc. GT19630 mediates the degradation of MYC, GSPT1, GSPT2, CK1 alpha, N-Myc, B7-H3 and XIAP, and disrupts the MYC-GSPT1 synergistic regulatory feedback loop. GT19630 inhibits cell proliferation, blocks S-phase progression of the cell cycle, promotes cell apoptosis, reduces cell migration capacity, induces integrated stress response, and blocks oxidative phosphorylation by inhibiting the TCA cycle. GT19630 can be used in the research of Myc-driven hematological cancers, small cell lung cancer, breast cancer, TP53-mutant cancers, and venetoclax-resistant cancers.
(Pink: c-Myc ligand (HY-168685); Blue: Cereblon ligand (HY-W093472); Black: linker (HY-W015808)).

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

Purity: 98.85%
CAS No.: 2883535-99-5
Formula: C₃₅H₃₀N₆O₅
Molecular Weight:614.65

Storage:

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

GT19630 Chemical Structure

CAS No.: 2883535-99-5

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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
- In Vitro
- In Vivo
Chemical Information
Solvent & Solubility
- In Vitro
- In Vivo
Purity & Documentation
References
Help & FAQs
Classifications
Bioz

Biological Activity

Description

GT19630 is an orally active c-Myc PROTAC targeted degrader based on the cereblon E3 ubiquitin ligase, with an IC₅₀ of 1.5 nM against human c-Myc. GT19630 mediates the degradation of MYC, GSPT1, GSPT2, CK1 alpha, N-Myc, B7-H3 and XIAP, and disrupts the MYC-GSPT1 synergistic regulatory feedback loop. GT19630 inhibits cell proliferation, blocks S-phase progression of the cell cycle, promotes cell apoptosis, reduces cell migration capacity, induces integrated stress response, and blocks oxidative phosphorylation by inhibiting the TCA cycle. GT19630 can be used in the research of Myc-driven hematological cancers, small cell lung cancer, breast cancer, TP53-mutant cancers, and venetoclax-resistant cancers^[1]^[2]^[3]^[4]^[5]. (Pink: c-Myc ligand (HY-168685); Blue: Cereblon ligand (HY-W093472); Black: linker (HY-W015808)).

IC₅₀ & Target^[1]^[2]^[3]^[4]^[5]

14390

1.5 nM (IC₅₀)

13593

14355

14391

14133

14392

XIAP

All PROTACs Isoforms :

All Casein Kinase Isoforms :

All IAP Isoforms :

In Vitro

GT19630 selectively degrades c-Myc protein in HL60 AML cells with an IC₅₀ of 1.5 nM, which is ~35-fold more potent than its activity in TF-1 erythroid progenitor cells (IC₅₀ = 52.5 nM)^[1].
GT19630 potently inhibits HL60 AML cell proliferation with an IC₅₀ of 0.33 nM, demonstrating >100-fold selectivity over normal myeloid bone marrow colony-forming cells (IC₅₀ = 40.2 nM) and ~79-fold selectivity over GM-CSF-stimulated TF-1 erythroid progenitor cells (IC₅₀ = 26.2 nM)^[1].
GT19630 (0.75-3 nM; 4-48 h) potently degrades MYC in BT549 and CAMA1 breast cancer cell lines, with degradation initiating at 0.75 nM (BT549) or 1.5 nM (CAMA1) by 48 h, and complete degradation achieved with 3 nM by 24 h^[2].
GT19630 (0-100 nM; 5 days) inhibits proliferation of 14 diverse human breast cancer cell lines with IC₅₀ values ranging from 1 to 100 nM, and exhibits consistent activity across major breast cancer molecular subtypes^[2].
GT19630 (0.75-3 nM; 48 h) downregulates XIAP protein expression in BT549, CAMA1, and MDA-MB-468 breast cancer cell lines following 48 h treatment with 0.75, 1.5, or 3 nM^[2].
GT19630 potently inhibits the proliferation of HL-60 acute myeloid leukemia cells with an IC₅₀ of 0.33 nM^[3].
GT19630 potently degrades c-Myc protein in HL-60 acute myeloid leukemia cells with an IC₅₀ of 1.5 nM, and this degradation is dependent on proteasome activity^[5].
GT19630 (salt form GT19715) potently inhibits HL-60 acute myeloid leukemia cell viability with an IC₅₀ of 1.8 nM^[5].
GT19630 selectively degrades GSPT1/GSPT2 (IC₉₀ <1 nM) and CK1α (IC₉₀ <10 nM) but does not degrade IKZF1/Ikaros in HL60 AML cells^[1].
GT19630 (100 µM down to serial 3-fold dilutions; 195 min total) binds to human CRBN with high affinity, exhibiting an IC₅₀ of 26.9 nM in an HTRF assay^[4].
GT19630 (10 nM; 8 h) induces proteasome-dependent, sustained degradation of both MYC and GSPT1 proteins in HL-60 AML cells at low nanomolar concentrations^[4].
GT19630 (variable concentrations; 24 h) induces significant stop-codon readthrough of MYC mRNA in HL-60 and HEK293T cells expressing a MYC-TGA-stop-EGFP reporter^[4].
GT19630 (1-5nM; 24 h) induces the integrated stress response in HL-60 GTS AML cells by upregulating ATF4 and ATF3 and activating stress-related gene pathways^[4].
GT19630 (5 nM; 12 h) potently inhibits oxidative phosphorylation and glycolysis in HL-60 GTS AML cells, reducing OCR, ECAR, and ATP-linked respiration^[4].
GT19630 (5 nM; 12 h) disrupts the TCA cycle in HL-60 GTS AML cells by reducing glutamine metabolism and citrate flux, leading to accumulation of glycolysis intermediates^[4].
GT19630 (5 nM; 12 h) decelerates TCA cycle flux in HL-60 GTS AML cells at the stages of glutamate synthesis and citrate synthesis, impairing mitochondrial respiration^[4].
GT19630 (variable concentrations; 48 h) induces potent, TP53-agnostic anti-proliferative and apoptotic effects in most blood cancer and SCLC cell lines (IC₅₀ <100 nM), with a therapeutic window relative to normal hematopoietic progenitors; efficacy is dependent on MYC degradation, with resistance in cells carrying a MYC^p.T58I mutation^[4].
GT19630 (64 nM; 72 h) induces greater cell death in AML LSPCs than normal NBM HSPCs, with TP53-agnostic activity, and reduces MYC protein levels more profoundly in AML LSPCs than normal HSPCs^[4].
Biotinylated GT19630 binds directly to c-Myc protein in a cell-free in vitro affinity purification assay^[5].
GT19630 (3-12 nM; 48 h) induces S phase cell cycle arrest in BT549, T47D, and MDA-MB-468 breast cancer cell lines following 48 h treatment with 3, 6, or 12 nM^[2].
GT19630 (3.1-10000 nM; 48 h) induces apoptosis in T47D, CAMA1, BT549, MDA-MB-468, HCC70, and SKBR3 breast cancer cell lines after 48 h, with greater activity in cell lines with lower proliferation IC₅₀ values^[2].
GT19630 (0.75-3 nM) degrades the negative immune checkpoint protein B7-H3 in BT549, CAMA1, and MDA-MB-468 breast cancer cell lines, with concentration-dependent reduction in protein levels and no effect on mRNA expression^[2].
GT19630 (3 nM; 24 h pre-treatment, 10-16 h migration) potently inhibits migration of BT549, CAMA1, and MDA-MB-468 breast cancer cell lines following 24 h pre-treatment with 3 nM, with the effect independent of apoptosis induction^[2].
GT19630 (low nanomolar concentrations) exerts multifunctional antitumor effects in breast cancer cell lines, including inhibition of proliferation, induction of apoptosis, suppression of migration, degradation of B7-H3, activation of the integrated stress response, and disruption of oxidative phosphorylation^[3].

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

Western Blot Analysis^[2]

Cell Line:

BT549, CAMA1 breast cancer cell lines
Concentration:

0.75-3 nM (48 h incubation); 3 nM (4, 8, 24 h incubation)
Incubation Time:

48 h (0.75, 1.5, 3 nM); 4, 8, 24 h (3 nM)
Result:

Induced concentration-dependent MYC degradation, with degradation beginning at 0.75 nM in BT549 cells and at 1.5 nM in CAMA1 cells after 48 h.
Began MYC degradation as early as 8 h in both cell lines with 3 nM treatment, with no visible MYC bands detected by 24 h.

Cell Proliferation Assay^[2]

Cell Line:

14 human breast cancer cell lines (luminal, HER2-positive, triple-negative subtypes)
Concentration:

0-100 nM
Incubation Time:

5 days
Result:

Inhibited cell proliferation across all 14 breast cancer cell lines, with IC50 values ranging from 1 to 100 nM.
Exhibited similar anti-proliferative activity across luminal, HER2-positive, and triple-negative breast cancer subtypes.

Cell Cycle Analysis^[2]

Cell Line:

BT549, T47D, MDA-MB-468 breast cancer cell lines
Concentration:

3-12 nM
Incubation Time:

48 h
Result:

Resulted in accumulation of cells in the S phase of the cell cycle in all three cell lines.
Decreased the proportion of cells in the G1/G0 and G2/M phases in all three cell lines tested.

Apoptosis Analysis^[2]

Cell Line:

T47D, CAMA1, BT549, MDA-MB-468, HCC70, SKBR3 breast cancer cell lines
Concentration:

3.1-12.5 nM (T47D, CAMA1, BT549, MDA-MB-468); 25-100 nM (HCC70); 2500-10000 nM (SKBR3)
Incubation Time:

48 h
Result:

Induced apoptosis in all six cell lines tested, with the extent of apoptosis dependent on cell line, concentration, and incubation time.
Showed greater susceptibility to apoptosis in cell lines with lower proliferation IC50 values (≤5 nM: T47D, CAMA1, BT549, MDA-MB-468), while cell lines with higher IC50 values (>40 nM: HCC70, SKBR3) were more resistant.

Western Blot Analysis^[2]

Cell Line:

BT549, CAMA1, MDA-MB-468 breast cancer cell lines
Concentration:

0.75-3 nM
Incubation Time:

48 h
Result:

Decreased XIAP protein expression in all three cell lines in a concentration-dependent manner.
Showed no consistent effect on XIAP mRNA expression across the cell lines.

Western Blot Analysis^[2]

Cell Line:

BT549, CAMA1, MDA-MB-468 breast cancer cell lines
Concentration:

0.75-3 nM (Western blot/ELISA); 3 nM (preliminary array screening)
Incubation Time:

48 h (preliminary array screening)
Result:

Decreased B7-H3 protein expression in all three cell lines in a concentration-dependent manner, as measured by both Western blot and ELISA.
Did not affect B7-H3 mRNA expression.

Cell Migration Assay ^[2]

Cell Line:

BT549, CAMA1, MDA-MB-468 breast cancer cell lines
Concentration:

3 nM
Incubation Time:

24 h pre-treatment; 10-16 h migration incubation
Result:

Significantly reduced cell migration in all three cell lines tested.
Showed the decreased migration was not due to apoptosis, as no significant apoptosis was observed over the migration assay time course.

Western Blot Analysis^[4]

Cell Line:

HL-60 AML cells (MYC-amplified)
Concentration:

10 nM (with 50 nM MLN9708); low nanomolar concentrations (dose-dependent)
Incubation Time:

8 h (with MLN9708); variable times (time-dependent); sustained up to 48 h post-washout
Result:

Profoundly reduced MYC protein levels, with this reduction completely rescued by co-treatment with proteasome inhibitors.
Reduced MYC in a dose- and time-dependent manner at low nanomolar concentrations, with reduced MYC levels sustained up to 48 hours after washout.
Degraded GSPT1 protein, unlike the selective GSPT1 degrader CC-90009 which did not affect MYC levels.

Western Blot Analysis^[4]

Cell Line:

HL-60 GT19630-sensitive (GTS) AML cells
Concentration:

1 nM; 2 nM; 5nM (western blotting); 5 nM (RNA-seq)
Incubation Time:

24 h (western blotting); 12 h (RNA-seq)
Result:

Upregulated ATF4 and ATF3 protein levels.
Led to significant upregulation of ISR, stress response, and endoplasmic reticulum stress pathways as revealed by RNA-seq and GSEA.

Cell Viability Assay^[4]

Cell Line:

diverse cancer cell lines (blood cancers, SCLCs, TNBCs, gliomas), normal erythroid or myeloid progenitors
Concentration:

variable concentrations
Incubation Time:

48 h
Result:

Inhibited proliferation of most blood cancer and SCLC cell lines with IC50 values below 100 nM.
Induced apoptosis with IC50 values ≤10 nM in most cell lines.
Showed higher IC50 values (43-44 nM) in normal erythroid or myeloid progenitors compared to cancer cell lines.
Exhibited TP53-agnostic efficacy in myeloid and lymphoid cell lines, except Raji Burkitt’s lymphoma cells (harboring a MYC p.T58I mutation) which were resistant.
Induced significantly greater apoptosis in MYC-overexpressing OCI-AML3 cells compared to control cells.

In Vivo

GT19630 (1-3 mg/kg; i.p.; twice daily) nearly eradicates Daudi lymphoma cells and significantly prolongs survival in NOD/SCID mice^[4].
GT19630 (0.1-1 mg/kg; i.p.; twice daily; i.p.; once daily (1 mg/kg)) significantly reduces HL-60 tumor volumes and MYC protein levels in BALB/c nude mice^[4].
GT19630 (0.3-3 mg/kg; i.p.; twice daily) significantly reduces MM.1S tumor volumes in NOD/SCID mice^[4].
GT19870 (3-12 mg/kg; p.o.; once daily) significantly reduces NCI H526 tumor volumes and MYC protein levels in BALB/c nude mice^[4].
GT19870 (3-12 mg/kg; p.o.; once daily) significantly reduces 22RV1 tumor volumes and MYC protein levels in BALB/c nude mice^[4].
GT19630 (3 mg/kg; i.p.; once daily) eradicates relapsed AML PDX cells in NOD/SCID mice^[4].
GT19630 (3 mg/kg; i.p.; three times weekly; 2 weeks on/1 week off cycles) reduces leukemia burden and prolongs survival by >300% in venetoclax-resistant MV4;11 AML in NSG mice^[4].
GT19630 (0.3 mg/kg; twice daily) degrades c-Myc and GSPT1 and inhibits tumor growth in an HL-60 acute myeloid leukemia xenograft model^[5].
GT19630 (3 mg/kg; i.p.; three times weekly; 2 weeks on/1 week off cycles) induces reversible myelosuppression with minimal body weight loss in humanized Crbn^I391V mice, with no observed mortality^[4].

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

Animal Model:

NOD/SCID mice^[4]
Dosage:

1 mg/kg; 3 mg/kg
Administration:

i.p.; twice daily
Result:

Nearly completely eradicated circulating CD20-positive cells.
Ensured 100% survival of mice on day 42 at 3 mg/kg dose, compared with 20% survival in vehicle-treated controls, resulting in significantly prolonged survival.

Animal Model:

BALB/c nude mice^[4]
Dosage:

0.1 mg/kg; 0.3 mg/kg; 1 mg/kg
Administration:

i.p.; twice daily (0.1, 0.3, 1 mg/kg); i.p.; once daily (1 mg/kg)
Result:

Reduced tumor volumes in a dose-dependent manner, with significant suppression across all treatment groups compared to vehicle.
Reduced MYC protein levels in tumors, with the reduction sustained for at least 24-48 hours after a single injection.

Animal Model:

NOD/SCID mice^[4]
Dosage:

0.3 mg/kg; 1 mg/kg; 3 mg/kg
Administration:

i.p.; twice daily
Result:

Significantly reduced MM.1S tumor volumes at all dose levels compared to vehicle, even below baseline.

Animal Model:

BALB/c nude mice (female, 4-6 weeks old)^[4]
Dosage:

3 mg/kg; 6 mg/kg; 12 mg/kg
Administration:

p.o.; once daily
Result:

Significantly reduced NCI H526 tumor volumes, with the 12 mg/kg group showing the strongest suppression.
Reduced MYC protein levels in tumors.

Animal Model:

BALB/c nude mice (female, 4-6 weeks old)^[4]
Dosage:

3 mg/kg; 6 mg/kg; 12 mg/kg
Administration:

p.o.; once daily
Result:

Significantly reduced 22RV1 tumor volumes, with the 6 mg/kg and 12 mg/kg groups showing strong suppression.
Reduced MYC protein levels in tumors.

Animal Model:

NOD/SCID mice^[4]
Dosage:

3 mg/kg
Administration:

i.p.; once daily
Result:

Eradicated AML cells in circulation, bone marrow, and spleens.
Resulted in significantly reduced spleen weights compared to vehicle treatment.

Animal Model:

NSG mice^[4]
Dosage:

3 mg/kg
Administration:

i.p.; three times weekly; 2 weeks on/1 week off cycles
Result:

Significantly reduced leukemia burden in both venetoclax-sensitive and venetoclax-resistant groups.
Profoundly reduced AML cells in bone marrow and spleens.
Greatly improved survival: median overall survival was prolonged from 37 days to 119 days in the venetoclax-resistant group, and treated venetoclax-sensitive mice had not reached median survival by study end.

Animal Model:

C57BL/6 CrbnWT mice; C57BL/6 CrbnI391V (humanized Crbn) mice^[4]
Dosage:

0.3 mg/kg; 3 mg/kg
Administration:

i.p.; three times weekly; 2 weeks on/1 week off cycles
Result:

Decreased MYC protein levels in bone marrow cells of CrbnI391V but not CrbnWT mice.
Decreased white blood cell counts in CrbnI391V mice treated with 3 mg/kg, while hemoglobin and platelet levels were unchanged.
Decreased body weights by a maximum of ~5% during treatment, with no deaths or obvious adverse events observed.
Increased murine bone marrow CD45-positive cells significantly post-treatment in CrbnI391V mice, suggesting recovery from myelosuppression.

Animal Model:

xenograft model^[5]
Dosage:

0.3 mg/kg
Administration:

twice daily
Result:

Degraded c-Myc and GSPT1 proteins.
Inhibited tumor growth.

Chemical Information

CAS No. 2883535-99-5
Appearance Solid
Molecular Weight 614.65
Formula C₃₅H₃₀N₆O₅
Color White to off-white
SMILES

O=C(C1=CC=C2C(N(C3C(NC(CC3)=O)=O)CC2=C1)=O)NCC4=CC=C(CNC(CN5C6=C(C7=CC=CC=C75)C=CC=N6)=O)C=C4
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

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

Solvent & Solubility

In Vitro:

DMSO : 100 mg/mL (162.69 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

1.6269 mL

8.1347 mL

16.2694 mL

5 mM

0.3254 mL

1.6269 mL

3.2539 mL

10 mM

0.1627 mL

0.8135 mL

1.6269 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.

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 90% Corn Oil

Solubility: ≥ 5 mg/mL (8.13 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:

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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.

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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

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (299 KB)
SDS (254 KB)
- English - EN (254 KB)
- Français - FR (254 KB)
- Deutsch - DE (254 KB)
- Norwegian - NO (254 KB)
- Español - ES (254 KB)
- Swedish - SV (254 KB)
- Italian - IT (254 KB)
- Korean - KR (254 KB)
- Portuguese - PT (254 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]. Ma L, et al. Abstract 5479: Discovery and evaluation of GT19630, a c-Myc/GSPT1 cereblon E3 ligase modulator (CELMoD), for targeting Myc-driven blood cancers and small cell lung cancers (SCLC). Cancer Res. 2022;82(12_Supplement):5479.

[2]. Tang M, et al. Targeting MYC for the treatment of breast cancer: use of the novel MYC-GSPT1 degrader, GT19630. Investigational new drugs. 2025 Feb;43(1):167-179. [Content Brief]

[3]. Lin Q, et al. Cancer Biology of GSPT1: Mechanisms and Targeted Therapy Opportunities of Molecular Glue Degraders. Advanced science (Weinheim, Baden-Wurttemberg, Germany). 2025 Dec;12(47):e11789. [Content Brief]

[4]. Nishida Y, et al. Dual MYC and GSPT1 Protein Degrader for MYC-Driven Cancers. bioRxiv. 2025 Apr 27.

[5]. Nishida Y, et al. C-MYC Targeting by Degradation: Novel Dual c-Myc/GSPT1 Degrader GT19715 Exerts Profound Cell Kill In Vitro and In Vivo in Acute Myeloid Leukemia and Lymphomas. AACR Annual Meeting 2022 Poster Abstract AML-147. 2022.

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	1.6269 mL	8.1347 mL	16.2694 mL	40.6736 mL
	5 mM	0.3254 mL	1.6269 mL	3.2539 mL	8.1347 mL
	10 mM	0.1627 mL	0.8135 mL	1.6269 mL	4.0674 mL
	15 mM	0.1085 mL	0.5423 mL	1.0846 mL	2.7116 mL
	20 mM	0.0813 mL	0.4067 mL	0.8135 mL	2.0337 mL
	25 mM	0.0651 mL	0.3254 mL	0.6508 mL	1.6269 mL
	30 mM	0.0542 mL	0.2712 mL	0.5423 mL	1.3558 mL
	40 mM	0.0407 mL	0.2034 mL	0.4067 mL	1.0168 mL
	50 mM	0.0325 mL	0.1627 mL	0.3254 mL	0.8135 mL
	60 mM	0.0271 mL	0.1356 mL	0.2712 mL	0.6779 mL
	80 mM	0.0203 mL	0.1017 mL	0.2034 mL	0.5084 mL
	100 mM	0.0163 mL	0.0813 mL	0.1627 mL	0.4067 mL

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GT19630

Bioactive Compound Library Max

Bioactive Compound Library

Apoptosis Compound Library

Cell Cycle/DNA Damage Compound Library

Immunology/Inflammation Compound Library

Metabolism/Protease Compound Library

Stem Cell Signaling Compound Library

Wnt/Hedgehog/Notch Compound Library

Anti-Cancer Compound Library

Anti-Aging Compound Library

Anti-Cardiovascular Disease Compound Library

Endoplasmic Reticulum Stress Compound Library

Glycolysis Compound Library

Orally Active Compound Library

Glutamine Metabolism Compound Library

Anti-Breast Cancer Compound Library

Anti-Lung Cancer Compound Library

Anti-Blood Cancer Compound Library

Anti-Cancer Metabolism Compound Library

Transcription Factor-Targeted Library

PROTAC Library

Cell Death Library

Anti-Drug-Resistant Compound Library

Anti-Hematopathy Compound Library

Multi-Target Compound Library

MCE Bioactive Compound Library

Protein Kinase Compound Library

Non-Alcoholic Fatty Liver Disease (NAFLD) Compound Library

Cell Proliferation Compound Library

Lactic Acid Metabolic Compound Library

High-Throughput Bioactive Compound Library

All PROTACs Isoforms

All Casein Kinase Isoforms

All IAP Isoforms

Biological Activity

Chemical Information

Solvent & Solubility

Purity & Documentation

References

Help & FAQs

Complete Stock Solution Preparation Table

GT19630 Related Classifications

HY-148837 Related Classifications