1. Apoptosis Cell Cycle/DNA Damage Epigenetics MAPK/ERK Pathway Stem Cell/Wnt
  2. Apoptosis Caspase CDK PARP Bcl-2 Family ERK
  3. Calactin

Calactin is a glycoside that can be isolated from Asclepias curassavica L.. Calactin activates caspase-3, caspase-8, caspase-9, and phosphorylates ERK. Calactin induces DNA damage, apoptosis, PARP cleavage, G2/M phase cell cycle arrest, shifts Bax/Bcl-2 expression, and shows anti-proliferation effects in leukemia cells. Calactin can be used for the research of leukemia.

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

Calactin

Calactin Chemical Structure

CAS No. : 20304-47-6

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Description

Calactin is a glycoside that can be isolated from Asclepias curassavica L.. Calactin activates caspase-3, caspase-8, caspase-9, and phosphorylates ERK. Calactin induces DNA damage, apoptosis, PARP cleavage, G2/M phase cell cycle arrest, shifts Bax/Bcl-2 expression, and shows anti-proliferation effects in leukemia cells. Calactin can be used for the research of leukemia[1].

IC50 & Target[1]

Caspase-3

 

Caspase-8

 

Caspase-9

 

CDK1/cyclinB1

 

Bcl-2

 

Bax

 

In Vitro

Calactin (0.065-1 μM; 0-24 h) exhibits dose-dependent and time-dependent cytotoxicity against human leukemia K562 and Molt-4 cells[1].
Calactin (0.15 μM; 0-24 h) induces G2/M phase cell cycle arrest in human leukemia K562 and Molt-4 cells by reducing the expression of Cyclin B1, Cdk1, and Cdc25C[1].
Calactin (0.15 μM; 0-24 h) induces DNA damage in human leukemia K562 and Molt-4 cells[1].
Calactin (0.15 μM; 0-24 h) induces apoptosis in human leukemia K562 and Molt-4 cells, and this apoptosis proceeds independently of caspase-3 activity[1].
Calactin (0.15 μM; 0-24 h) induces apoptosis in human leukemia K562 and Molt-4 cells through both intrinsic and extrinsic apoptotic pathways[1].
Calactin (0.15 μM; 12 h) upregulates c-Fos mRNA expression in K562 and Molt-4 cells via the ERK signaling pathway[1].

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

Cell Viability Assay[1]

Cell Line: human leukemia K562 and Molt-4 cells
Concentration: 0.065, 0.125, 0.15, 0.25, 0.5, 1 μM
Incubation Time: 0, 6, 12, 24 h
Result: Reduced cell viability in a dose-dependent and time-dependent manner.
Exhibited a LD50 of 0.161 μM for K562 cells after 12 h treatment.
Exhibited a LD50 of 0.142 μM for Molt-4 cells after 12 h treatment.
Caused progressively decreased cell viability relative to untreated controls when used at 0.15 μM for 6, 12, 18, and 24 h.

Cell Cycle Analysis[1]

Cell Line: human leukemia K562 and Molt-4 cells
Concentration: 0.15 μM
Incubation Time: 0, 6, 12, 24 h
Result: Induced a significant increase in the percentage of K562 cells arrested at the G2/M phase, from 12.8% at 0 h to 34.4% at 24 h.
Reduced the expression levels of Cyclin B1, Cdk1, and Cdc25C in both cell lines over the 24 h treatment period.

Western Blot Analysis[1]

Cell Line: human leukemia K562 and Molt-4 cells
Concentration: 0.15 μM
Incubation Time: 0, 6, 12, 24 h
Result: Increased phosphorylation levels of Chk2 and H2AX in a time-dependent manner.
Showed no change in total Chk2 or H2AX protein expression.

Apoptosis Analysis[1]

Cell Line: human leukemia K562 and Molt-4 cells
Concentration: 0.15 μM
Incubation Time: 0, 6, 12, 24 h
Result: Caused a significant increase in apoptotic cells after treatment.
Did not block calactin-induced phosphatidylserine exposure when cells were pretreated with Z-DEVD-FMK, indicating no reduction in apoptotic cell levels.

Western Blot Analysis[1]

Cell Line: human leukemia K562 and Molt-4 cells
Concentration: 0.15 μM
Incubation Time: 0, 6, 12, 24 h
Result: Induced PARP cleavage in both cell lines over the 24 h treatment period.
Increased levels of active caspase-3, caspase-8, caspase-9, and Bax in both cell lines over the 24 h treatment period.
Decreased levels of procaspase-3, procaspase-8, procaspase-9, and Bcl-2 in both cell lines over the 24 h treatment period.
Increased phosphorylation levels of ERK and Elk-1 in a time-dependent manner, with no change in total ERK or Elk-1 protein expression.
Molecular Weight

532.63

Formula

C29H40O9

CAS No.
SMILES

C(=O)[C@@]12[C@@]3([C@]([C@]4(O)[C@](C)(CC3)[C@H](CC4)C5=CC(=O)OC5)(CC[C@]1(C[C@@]6([C@@](C2)(O[C@]7(O)[C@](O6)(O[C@H](C)C[C@H]7O)[H])[H])[H])[H])[H])[H]

Structure Classification
Initial Source
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Room temperature in continental US; may vary elsewhere.

Storage

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

Purity & Documentation
References
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Calactin
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HY-167237
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