Art. -Nr.: HY-10996A

KHS101 hydrochloride

2 Cited Publications

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Based on 2 publication(s) in Google Scholar

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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Reinheit: 99.65%
CAS. Nr.: 1784282-12-7
Formel: C₁₈H₂₂ClN₅S
Molecular Weight:375.92

Speicherung:

4°C, sealed storage, away from moisture

* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

KHS101 hydrochloride Chemical Structure

CAS. Nr.: 1784282-12-7

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Biologische Aktivität
- Beschreibung
- IC₅₀ & Target
- In Vitro
- In Vivo
Chemical Information
Publications (2)
Lösungsmittel & Löslichkeit
- In Vitro
- In Vivo
Reinheit & Dokumentation
Verweise
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

IC₅₀ & Target

TACC3^[1]

Alle Aurora Kinase Isoform-spezifische Produkte anzeigen :

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

Alle HSP Isoform-spezifische Produkte anzeigen :

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, 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.

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. 1784282-12-7
Appearance Solid
Molecular Weight 375.92
Formel C₁₈H₂₂ClN₅S
Color White to off-white
SMILES

[H]Cl.CC(CNC1=NC(NCC2=CSC(C3=CC=CC=C3)=N2)=NC=C1)C
Versand

Room temperature in continental US; may vary elsewhere.
Speicherung

4°C, sealed storage, away from moisture

* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

Publications (2)

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bioRxiv

2026 Apr 29.
University of Califomia San Francisco

2026.

Lösungsmittel & Löslichkeit

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)

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

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

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.

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: ≥ 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.

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.

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:

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

Reinheit & Dokumentation

Select Batch:

Reinheit: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (295 KB)
SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
- Norwegian - NO (393 KB)
- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Korean - KR (393 KB)
- Portuguese - PT (393 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)

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]

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

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
H₂O / DMSO	1 mM	2.6601 mL	13.3007 mL	26.6014 mL	66.5035 mL
	5 mM	0.5320 mL	2.6601 mL	5.3203 mL	13.3007 mL
	10 mM	0.2660 mL	1.3301 mL	2.6601 mL	6.6504 mL
	15 mM	0.1773 mL	0.8867 mL	1.7734 mL	4.4336 mL
	20 mM	0.1330 mL	0.6650 mL	1.3301 mL	3.3252 mL
	25 mM	0.1064 mL	0.5320 mL	1.0641 mL	2.6601 mL
DMSO	30 mM	0.0887 mL	0.4434 mL	0.8867 mL	2.2168 mL
	40 mM	0.0665 mL	0.3325 mL	0.6650 mL	1.6626 mL
	50 mM	0.0532 mL	0.2660 mL	0.5320 mL	1.3301 mL
	60 mM	0.0443 mL	0.2217 mL	0.4434 mL	1.1084 mL
	80 mM	0.0333 mL	0.1663 mL	0.3325 mL	0.8313 mL
	100 mM	0.0266 mL	0.1330 mL	0.2660 mL	0.6650 mL

* 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.

Keywords

KHS101 hydrochloride

2 Cited Publications

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KHS101 hydrochloride

Apoptosis Compound Library

Cell Cycle/DNA Damage Compound Library

Epigenetics Compound Library

Kinase Inhibitor Library

Metabolism/Protease Compound Library

Anti-Cancer Compound Library

CNS-Penetrant Compound Library

Autophagy Compound Library

Anti-Aging Compound Library

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Publications Citing Use of MedChemExpress (MCE) KHS101 hydrochloride

Alle Aurora Kinase Isoform-spezifische Produkte anzeigen

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

Alle HSP Isoform-spezifische Produkte anzeigen

Biologische Aktivität

Chemical Information

Publications (2)

Lösungsmittel & Löslichkeit

Reinheit & Dokumentation

Verweise

Help & FAQs

Complete Stock Solution Preparation Table

KHS101 hydrochloride Related Classifications

HY-10996A Related Classifications