Art. -Nr.: HY-10996

KHS101

2 Cited Publications

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KHS101 is a blood-brain barrier-penetrant anticancer agent that primarily functions by inhibiting HSPD1 (IC₅₀ = 14.4 μM) and TACC3 across different cellular backgrounds. KHS101 promotes the aggregation of HSPD1 with client proteins, destabilizes TACC3, and reduces the levels of TACC3, Aurora A and PLK1. KHS101 induces autophagy, apoptosis, cell cycle exit and neuronal differentiation; it suppresses cancer cell growth, motility, EMT and stemness; it also impairs mitochondrial bioenergetics and glycolysis in glioblastoma cells. KHS101 can be used in research related to glioblastoma multiforme and breast cancer.

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CAS. Nr.: 1262770-73-9
Formel: C₁₈H₂₁N₅S
Molecular Weight:339.46

Speicherung:

Please store the product under the recommended conditions in the Certificate of Analysis.

Data Sheet (294 KB)

KHS101 Chemical Structure

CAS. Nr.: 1262770-73-9

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Biologische Aktivität
- Beschreibung
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Publications (2)
Reinheit & Dokumentation
Verweise
Calculators
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Bioz

Biologische Aktivität

Beschreibung

Alle HSP Isoform-spezifische Produkte anzeigen :

Alle Aurora Kinase Isoform-spezifische Produkte anzeigen :

Alle Polo-like Kinase (PLK) Isoform-spezifische Produkte anzeigen :

Cellular Effect

Cell Line	Type	Value	Description	References
JIMT-1	IC₅₀	32.98 μM Compound: 7a	Antiproliferative activity against human JIMT-1 cells assessed as cell growth inhibition measured after 72 hrs by MTT assay Antiproliferative activity against human JIMT-1 cells assessed as cell growth inhibition measured after 72 hrs by MTT assay	[PMID: 36332551]
MDA-MB-231	IC₅₀	31.13 μM Compound: 7a	Antiproliferative activity against human MDA-MB-231 cells assessed as cell growth inhibition measured after 72 hrs by MTT assay Antiproliferative activity against human MDA-MB-231 cells assessed as cell growth inhibition measured after 72 hrs by MTT assay	[PMID: 36332551]
SK-OV-3	IC₅₀	21.44 μM Compound: 7a	Antiproliferative activity against human SK-OV-3 cells assessed as cell growth inhibition measured after 72 hrs by MTT assay Antiproliferative activity against human SK-OV-3 cells assessed as cell growth inhibition measured after 72 hrs by MTT assay	[PMID: 36332551]
U-251	IC₅₀	49.13 μM Compound: 7a	Cytotoxicity against human U251 cells assessed as inhibition of cell growth measured after 72 hrs by MTT assay Cytotoxicity against human U251 cells assessed as inhibition of cell growth measured after 72 hrs by MTT assay	[PMID: 36332551]
U-87MG ATCC	IC₅₀	37.85 μM Compound: 7a	Antiproliferative activity against human U87 cells assessed as inhibition of cell growth incubated for 72 hrs by MTT assay Antiproliferative activity against human U87 cells assessed as inhibition of cell growth incubated for 72 hrs by MTT assay	[PMID: 36332551]

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.

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, GBM11, 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^[2]

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, SKBR3, and MCF7 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.

In Vivo

KHS101 (6 mg/kg; subcutaneous injection; twice daily; for 10 consecutive days) reduces the proliferation, invasion and spread of GBM tumors in intracranial patient-derived xenograft mouse models without obvious toxicity^[1].
KHS101 (6 mg/kg; subcutaneous injection; twice daily; alternating 3 or 5 days of administration per week for a total of 10 weeks) significantly improves the survival rate and reduces tumor volume in GBMX1 intracranial xenograft mouse models, with no obvious toxicity^[1].
KHS101 (6 mg/kg; subcutaneous injection; twice daily for 14 consecutive days) significantly increases the neuronal differentiation level of endogenous neural progenitor cells in adult rats, elevating the proportion of BrdU/NeuN double-positive cells from approximately 20% to approximately 40%. Meanwhile, it reduces the proliferative capacity of neural progenitor cells without inducing apoptosis or causing obvious toxicity^[3].

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

Animal Model:

Immunodeficient mice^[1]
Dosage:

6 mg/kg
Administration:

s.c.; twice daily; 10 days
Result:

Increased NAD(P)H autofluorescence signal area in tumor tissue.
Increased HK2-positive tumor area.
Reduced tumor cell proliferation by ~2-fold (assessed by MKI67 staining).
Increased acellular/pyknotic areas in tumor sections.
Reduced frontal-to-caudal tumor expansion across sequential brain sections.
Reduced vimentin-positive tumor cell invasion across the corpus callosum by ≥ 2-fold.
Showed no discernible hepatic toxicity.

Animal Model:

Immunodeficient mice^[1]
Dosage:

6 mg/kg
Administration:

s.c.; twice daily; biweekly alternating 5 and 3 treatment days per week for 10 weeks
Result:

Increased survival of GBMX1 tumor-bearing mice in both cohorts.
Reduced tumor size by ~2-fold compared with vehicle-treated mice.
Showed no treatment-related adverse effects leading to study removal.

Animal Model:

Fisher 344 (adult, ~10 weeks old)^[3]
Dosage:

6 mg/kg
Administration:

s.c.; twice daily; 14 days
Result:

Increased the percentage of BrdU/NeuN double-positive cells from ~20% to ~40% in the hippocampal dentate gyrus.
Significantly reduced the number of Ki67-positive cells and BrdU-positive cells in the subgranular layer of the dentate gyrus.
Showed no significant difference in the percentage of BrdU/GFAP double-positive cells.
Left apoptosis (assessed via cleaved caspase 3 staining) in the dentate gyrus unchanged compared to vehicle controls.
Caused no signs of lethargy, weight loss, or sickness in treated animals.

Chemical Information

CAS. Nr. 1262770-73-9
Molecular Weight 339.46
Formel C₁₈H₂₁N₅S
SMILES

CC(C)CNC1=NC(NCC2=CSC(C3=CC=CC=C3)=N2)=NC=C1
Versand

Room temperature in continental US; may vary elsewhere.
Speicherung

Please store the product under the recommended conditions in the Certificate of Analysis.

Publications (2)

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bioRxiv

2026 Apr 29.
University of Califomia San Francisco

2026.

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Reinheit: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (294 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)
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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]. Polson ES, et al. KHS101 disrupts energy metabolism in human glioblastoma cells and reduces tumor growth in mice. Sci Transl Med. 2018;10(454):eaar2718. [Content Brief]

[2]. Campo L, et al. Inhibition of TACC3 by a small molecule inhibitor in breast cancer. Biochem Biophys Res Commun. 2018;498(4):1085-1092. [Content Brief]

[3]. Wurdak H, et al. A small molecule accelerates neuronal differentiation in the adult rat. Proc Natl Acad Sci U S A. 2010;107(38):16542-16547. [Content Brief]

Calculators

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

Mass Mass

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Volumen Volumen

Molecular Weight Molecular Weight

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

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

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

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

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

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KHS101

2 Cited Publications

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KHS101

Publications Citing Use of MedChemExpress (MCE) KHS101

Alle HSP Isoform-spezifische Produkte anzeigen

Alle Aurora Kinase Isoform-spezifische Produkte anzeigen

Alle Polo-like Kinase (PLK) Isoform-spezifische Produkte anzeigen

Biologische Aktivität

Chemical Information

Publications (2)

Reinheit & Dokumentation

Verweise

Calculators

Help & FAQs

KHS101 Related Classifications

HY-10996 Related Classifications