| In Vitro |
KHS101 (0-20 μM; 5 days) induces dose-dependent cytotoxicity in all 6 patient-derived GBM cell lines as well as U251/U87 cells, with IC50 values at 5 days of treatment as follows: 2.23 μM in GBM1 cells, 0.97 μM in GBM4 cells, 5.05 μM in GBM11 cells, 3.28 μM in GBM13 cells, 1.98 μM in GBM14 cells, and 1.87 μM in GBM20 cells[1].
Treatment with KHS101 (1-7.5 μM; 12 h) selectively induces concentration-dependent autophagy in patient-derived human glioblastoma (GBM) cell lines (GBM1, GBM4, GBM11, GBM13, GBM14, GBM20), whereas no observable effect is detected in non-cancerous NP1 neural progenitor cells[1].
KHS101 (7.5 μM; 48 h) selectively induces time-dependent apoptosis in patient-derived human GBM cell lines (GBM1, GBM11, GBM20), while exerting minimal effects on non-cancerous NP1 neural progenitor cells, and this apoptosis is independent of late-stage autophagy[1].
KHS101 (7.5 μM) selectively disrupts the metabolic phenotype of patient-derived human GBM cell lines and induces a significant hypoxic shift in metabolic activity, whereas acute treatment at 7.5 μM causes only minimal glycolytic changes in non-cancerous cell lines (NP1, NP2, NHAs)[1].
KHS101 (7.5 μM; 4-24 h) selectively impairs aerobic glycolysis and tricarboxylic acid (TCA) cycle activity in patient-derived human GBM1 cells, reduces the incorporation of glucose-derived carbon into key metabolic intermediates, and decreases total cellular ATP levels by ≥ 50% after 24 hours; this agent exerts no such effects in non-cancerous NP1 neural progenitor cells[1].
KHS101 (7.5 μM; 1 h) selectively induces the aggregation of HSPD1 and key metabolic enzymes in patient-derived human GBM1 cells, whereas only minimal aggregation is observed in non-cancerous NP1 neural progenitor cells[1].
KHS101 (10-100 μM; 24 h) inhibits the proliferation of MDA-MB-231, MDA-MB-468 and MCF7 breast cancer cells in a TACC3 expression-dependent manner, with 20 μM selectively suppressing the growth of breast cancer cells without affecting the non-tumorigenic mammary epithelial cell line MCF10A[2].
KHS101 (5-20 μM; 24 h) reduces TACC3 protein levels in MDA-MB-231 and SKBR3 breast cancer cells at the concentration of 20 μM, but does not alter TACC3 levels in MDA-MB-468 and BT549 breast cancer cells after 24 h of treatment[2].
KHS101 (5-20 μM; 7 days) inhibits mammosphere formation and reduces mammosphere formation efficiency in MDA-MB-468 and SKBR3 breast cancer cells[2].
KHS101 (5-20 μM; 24 h) reduces the mRNA expression levels of the stem cell markers Oct4, Sox2 and Nanog in MDA-MB-231 breast cancer cells[2].
KHS101 (20 μM; 24 h) reduces the protein expression levels of mesenchymal markers (N-cadherin, Vimentin) and the stemness marker CD44 in MDA-MB-231 breast cancer cells[2].
KHS101 (20 μM; 24 h) reduces the mRNA expression levels of EMT transcription factors including Snail, Slug and Twist in MDA-MB-231 breast cancer cells[2].
KHS101 (20-60 μM; 16 h) inhibits the migration of MDA-MB-231 and MDA-MB-468 breast cancer cells[2].
KHS101 (20 μM; 24 h) inhibits the invasion of MDA-MB-231 and MDA-MB-468 breast cancer cells after treatment at 20 μM for 24 h[2].
KHS101 (20 μM; 24-72 h) increases the sub-G1 phase apoptotic cell population in MDA-MB-231 and MDA-MB-468 breast cancer cells after treatment at 20 μM for 24, 48, and 72 h, and exerts cell type-specific effects on the overall cell cycle distribution[2].
KHS101 (20 μM; 24-72 h) induces time-dependent apoptosis in MDA-MB-231 and MDA-MB-468 breast cancer cells after treatment at 20 μM for 24, 48, and 72 h, with a stronger effect on MDA-MB-468 cells[2].
KHS101 (20 μM) alters the global proteomic profile of MDA-MB-468 breast cancer cells, with significant changes observed in proteins involved in catalytic activity, binding, metabolic processes, cellular processes, and multiple cancer-related signaling pathways[2].
KHS101 (20 μM; 24 h) reduces the protein expression of Aurora A and PLK1 mitotic kinases in MDA-MB-468, SKBR3 and MCF7 breast cancer cells[2].
KHS101 (0.6-5 μM; 1-12 d) induces neuronal differentiation of adherently cultured adult rat hippocampal neural progenitor cells (NPCs) in a dose-dependent manner, with an EC50 of approximately 1 μM; treatment at 5 μM for 12 days generates functionally mature neurons[3].
KHS101 (1.5-5 μM; 4 d) induces neuronal differentiation of secondary neurospheres derived from neural precursor cells (NPCs) in the hippocampus and SVZ of adult rats. Under the condition of treatment with 1.5-5 μM for 4 days, 40%-60% of the cells become TuJ1-positive neurons[3].
KHS101 (0.6-5 μM; 4 d) dose-dependently inhibits BMP4-induced differentiation of adult rat hippocampal neural precursor cells (NPCs) into astrocytes and promotes their differentiation into neurons[3].
KHS101 (0.6-5 μM; 24 h-72 h) upregulates the expression of Cdkn1 in a dose-dependent manner, and inhibits the proliferation and mitotic activity of neural precursor cells (NPCs) in the hippocampus of adult rats; after treatment with 5 μM for 72 h, the number of Ki67-positive cells decreases significantly[3].
KHS101 (5-15 μM; 12-24 h) enhances the nuclear localization of ARNT2 in ectopically expressing 293T cells and adult rat hippocampal neural precursor cells (NPCs)[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
KHS101 hydrochloride Related Antibodies
Cell Autophagy Assay[1]
| Cell Line: |
Patient-derived human GBM cell lines (GBM1, GBM4, GBM11, GBM13, GBM14, GBM20), noncancerous adult brain neural progenitor (NP1) cell line |
| Concentration: |
1 μM, 2.5 μM, 7.5 μM |
| Incubation Time: |
12 h |
| Result: |
Induced pronounced intracellular vacuole development and increased LC3B-positive autophagosomal compartments in GBM1 cells compared to NP1 cells and vehicle-treated controls after 12 hours of treatment with 7.5 μM.
Increased LC3B staining in all tested GBM cell lines, while NP1 cells showed no such increase.
Caused concentration-dependent increase in LC3B-positive cytoplasmic area in GBM1, GBM11, and GBM20 cells after 12 hours, with the highest response at 7.5 μM.
Increased CYTO-ID positive cells in GBM1 cells in a concentration-dependent manner, with > 80% of cells positive after 12 hours of treatment with 7.5 μM. |
Apoptosis Analysis[1]
| Cell Line: |
Patient-derived human GBM cell lines (GBM1, GBM4, GBM11, GBM13, GBM14, GBM20), noncancerous adult brain neural progenitor (NP1) cell line |
| Concentration: |
7.5 μM |
| Incubation Time: |
48 h |
| Result: |
Induced a time-dependent increase in caspase 3/7 activation in GBM1 cells over 50 hours, with significantly higher activation than vehicle controls at the 48-hour time point.
Caused marked increases in relative caspase 3/7 activation in GBM1, GBM11, and GBM20 cells compared to NP1 cells after 48 hours of treatment with 7.5 μM.
Induced significant accumulation of annexin V-positive apoptotic cells in GBM1 cells 48 hours after treatment, and this apoptotic cell death was not prevented by chemical inhibition of late-stage autophagy. |
Cell Proliferation Assay[1]
| Cell Line: |
MCF10A non-tumorigenic human mammary epithelial cells, MDA-MB-231, MDA-MB-468, and MCF7 breast cancer cells |
| Concentration: |
10, 20, 40, 60, 80, 100 μM |
| Incubation Time: |
24 h |
| Result: |
Showed breast cancer cells (MDA-MB-231, MDA-MB-468, MCF7) were more sensitive to KHS101 than MCF10A cells, with proliferation inhibition correlated to endogenous TACC3 expression.
Revealed MDA-MB-231 and MDA-MB-468 (high TACC3) showed greater sensitivity than MCF7 (low/undetectable TACC3).
Suppressed breast cancer cell growth at 20 μM but did not affect MCF10A cell growth. |
Western Blot Analysis[2]
| Cell Line: |
MDA-MB-231, MDA-MB-468, SKBR3, and BT549 breast cancer cells |
| Concentration: |
5, 10, 20 μM |
| Incubation Time: |
24 h |
| Result: |
Significantly reduced TACC3 protein levels at 20 μM in MDA-MB-231 and SKBR3 cells.
Showed no significant change in TACC3 levels in MDA-MB-468 and BT549 cells. |
Real Time qPCR[2]
| Cell Line: |
MDA-MB-231 breast cancer cells |
| Concentration: |
5, 10, 20 μM |
| Incubation Time: |
24 h |
| Result: |
Reduced mRNA expression of stem cell markers Oct4, Sox2, and Nanog in a concentration-dependent manner.
Showed all tested concentrations significantly decreased marker expression relative to control. |
Western Blot Analysis[2]
| Cell Line: |
MDA-MB-468 and MDA-MB-231 breast cancer cells |
| Concentration: |
20 μM |
| Incubation Time: |
24 h |
| Result: |
Reduced protein expression of mesenchymal markers N-cadherin and Vimentin, and stemness marker CD44 in MDA-MB-231 cells.
Found MDA-MB-468 cells showed undetectable N-cadherin and CD44 levels, and reduced TACC3 expression. |
Real Time qPCR[2]
| Cell Line: |
MDA-MB-231 breast cancer cells |
| Concentration: |
20 μM |
| Incubation Time: |
24 h |
| Result: |
Significantly reduced mRNA expression of EMT transcription factors Snail, Slug, and Twist relative to control. |
Cell Migration Assay [2]
| Cell Line: |
MDA-MB-231 and MDA-MB-468 breast cancer cells |
| Concentration: |
20, 40, 60 μM |
| Incubation Time: |
16 h |
| Result: |
Reduced relative migration of MDA-MB-231 and MDA-MB-468 cells in a concentration-dependent manner.
Showed all tested concentrations significantly decreased migration relative to control. |
Cell Invasion Assay[2]
| Cell Line: |
MDA-MB-231 and MDA-MB-468 breast cancer cells |
| Concentration: |
20 μM |
| Incubation Time: |
24 h |
| Result: |
Significantly reduced relative invasion of MDA-MB-231 and MDA-MB-468 cells relative to control. |
Cell Cycle Analysis[2]
| Cell Line: |
MDA-MB-231 and MDA-MB-468 breast cancer cells |
| Concentration: |
20 μM |
| Incubation Time: |
24, 48, 72 h |
| Result: |
Induced cell cycle distribution changes in a cell type-dependent manner.
Significantly increased the sub-G1 population (a marker of apoptotic cells) in both MDA-MB-231 and MDA-MB-468 cells in a time-dependent manner. |
Apoptosis Analysis[2]
| Cell Line: |
MDA-MB-231 and MDA-MB-468 breast cancer cells |
| Concentration: |
20 μM |
| Incubation Time: |
24, 48, 72 h |
| Result: |
Increased the percentage of apoptotic cells in both MDA-MB-231 and MDA-MB-468 cells in a time-dependent manner.
Found MDA-MB-468 cells showed a greater magnitude of apoptotic induction than MDA-MB-231 cells. |
Western Blot Analysis[2]
| Cell Line: |
MDA-MB-468 and MDA-MB-231 breast cancer cells |
| Concentration: |
20 μM |
| Incubation Time: |
24 h |
| Result: |
Significantly reduced protein expression of mitotic kinases Aurora A and PLK1 in MDA-MB-468, SKBR3, and MCF7 cells, regardless of endogenous TACC3 expression levels. |
|
| Solvent & Solubility |
In Vitro:
DMSO : 160 mg/mL (425.62 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
H2O : 10 mg/mL (26.60 mM; ultrasonic and warming and heat to 60°C)
Preparing
Stock Solutions
|
Concentration
Solvent
Mass
|
1 mg |
5 mg |
10 mg |
|
1 mM
|
2.6601 mL
|
13.3007 mL
|
26.6014 mL
|
|
5 mM
|
0.5320 mL
|
2.6601 mL
|
5.3203 mL
|
|
10 mM
|
0.2660 mL
|
1.3301 mL
|
2.6601 mL
|
View the 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 (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
*
Note: If you choose water as the stock solution, please dilute it to the working solution,
then filter and sterilize it with a 0.22 μm filter before use.
Molarity CalculatorDilution Calculator
Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
This equation is commonly abbreviated as: C1V1 = C2V2
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.
-
Protocol 1
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline Solubility: ≥ 2.67 mg/mL (7.10 mM); Clear solution
This protocol yields a clear solution of ≥ 2.67 mg/mL (saturation unknown). Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (26.7 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.
-
Protocol 2
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline) Solubility: ≥ 2.67 mg/mL (7.10 mM); Clear solution
This protocol yields a clear solution of ≥ 2.67 mg/mL (saturation unknown). Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (26.7 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
-
Protocol 3
Add each solvent one by one: 10% DMSO 90% Corn Oil Solubility: ≥ 2.67 mg/mL (7.10 mM); Clear solution
This protocol yields a clear solution of ≥ 2.67 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 (26.7 mg/mL) to 900 μL Corn oil, and mix evenly.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
Please enter your animal formula composition:
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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).
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