Cat. No.: HY-119831

Rohitukine

Rohitukine is an orally active CDK9/T1 inhibitor with an IC₅₀of 0.3 μM. Rohitukine blocks ATP binding sites of CDK2/A and CDK9/T1, suppresses PPARγ, AKT, mTOR, C/EBPα, SREBP-2, and NF-κB signaling, and increases hepatic LXRα expression. Rohitukine induces S-phase cell cycle arrest, ROS generation, apoptosis, and exhibits anti-inflammatory activity. Rohitukine can be used for the research of leukemia, pancreatic cancer, prostate cancer, breast cancer, CNS cancer, ovarian cancer, lung cancer, dyslipidemia, inflammatory diseases, inflammatory bowel disease, and arthritis.

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CAS No.: 71294-60-5
화학식: C₁₆H₁₉NO₅
분자량:305.33

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

Data Sheet (298 KB)

Rohitukine Chemical Structure

CAS No.: 71294-60-5

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Biological Activity
- 제품 설명
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
순도&문서
References
Calculators
Help & FAQs
Classifications
Bioz

Biological Activity

제품 설명

IC₅₀ & Target^[1]

CDK2/A

7.5 μM (IC₅₀)

CDK9/T1

0.3 μM (IC₅₀)

All NF-κB Isoforms :

All CDK Isoforms :

All PPAR Isoforms :

All Akt Isoforms :

All mTOR Isoforms :

All Wnt Isoforms :

All Interleukin Related Isoforms :

All p38 MAPK Isoforms :

All ERK Isoforms :

All JNK Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
A549	IC₅₀	>10 μM Compound: 5	Cytotoxicity against human A549 cells after 48 hrs by MTT assay Cytotoxicity against human A549 cells after 48 hrs by MTT assay	[PMID: 19757855]
ASPC1	GI₅₀	21 μM Compound: 1	Cytotoxicity against human AsPC1 cells assessed as cell growth inhibition after 48 hrs by MTT assay Cytotoxicity against human AsPC1 cells assessed as cell growth inhibition after 48 hrs by MTT assay	[PMID: 27363938]
BXPC-3	GI₅₀	20 μM Compound: 1	Cytotoxicity against human BxPC3 cells assessed as cell growth inhibition after 48 hrs by MTT assay Cytotoxicity against human BxPC3 cells assessed as cell growth inhibition after 48 hrs by MTT assay	[PMID: 27363938]
Caco-2	GI₅₀	25 μM Compound: 1	Growth inhibition of human Caco2 cells after 48 hrs by MTT assay Growth inhibition of human Caco2 cells after 48 hrs by MTT assay	[PMID: 29370702]
DU-145	GI₅₀	26 μM Compound: 1	Cytotoxicity against human DU145 cells assessed as cell growth inhibition after 48 hrs by MTT assay Cytotoxicity against human DU145 cells assessed as cell growth inhibition after 48 hrs by MTT assay	[PMID: 27363938]
HCT-116	IC₅₀	8.8 μM Compound: 5	Cytotoxicity against human HCT116 cells after 48 hrs by MTT assay Cytotoxicity against human HCT116 cells after 48 hrs by MTT assay	[PMID: 19757855]
HEK293	GI₅₀	>50 μM Compound: 1	Cytotoxicity against HEK293 cells assessed as cell growth inhibition after 48 hrs by MTT assay Cytotoxicity against HEK293 cells assessed as cell growth inhibition after 48 hrs by MTT assay	[PMID: 27363938]
HL-60	GI₅₀	10 μM Compound: 1	Cytotoxicity against human HL60 cells assessed as cell growth inhibition after 48 hrs by MTT assay Cytotoxicity against human HL60 cells assessed as cell growth inhibition after 48 hrs by MTT assay	[PMID: 27363938]
HL-60	GI₅₀	10 μM Compound: 1	Growth inhibition of human HL60 cells after 48 hrs by MTT assay Growth inhibition of human HL60 cells after 48 hrs by MTT assay	[PMID: 29370702]
HL-60	IC₅₀	7.5 μM Compound: 5	Cytotoxicity against human HL60 cells after 48 hrs by MTT assay Cytotoxicity against human HL60 cells after 48 hrs by MTT assay	[PMID: 19757855]
Hs-578T	GI₅₀	20 μM Compound: 1	Cytotoxicity against human Hs578T cells assessed as cell growth inhibition after 48 hrs by MTT assay Cytotoxicity against human Hs578T cells assessed as cell growth inhibition after 48 hrs by MTT assay	[PMID: 27363938]
K562	GI₅₀	24 μM Compound: 1	Cytotoxicity against human K562 cells assessed as cell growth inhibition after 48 hrs by MTT assay Cytotoxicity against human K562 cells assessed as cell growth inhibition after 48 hrs by MTT assay	[PMID: 27363938]
LNCaP	GI₅₀	30 μM Compound: 1	Cytotoxicity against human LNCAP cells assessed as cell growth inhibition after 48 hrs by MTT assay Cytotoxicity against human LNCAP cells assessed as cell growth inhibition after 48 hrs by MTT assay	[PMID: 27363938]
MCF7	GI₅₀	28 μM Compound: 1	Growth inhibition of human MCF7 cells after 48 hrs by MTT assay Growth inhibition of human MCF7 cells after 48 hrs by MTT assay	[PMID: 29370702]
MCF7	IC₅₀	>10 μM Compound: 5	Cytotoxicity against human MCF7 cells after 48 hrs by MTT assay Cytotoxicity against human MCF7 cells after 48 hrs by MTT assay	[PMID: 19757855]
MDA-MB-231	GI₅₀	13 μM Compound: 1	Cytotoxicity against human MDA-MB-231 cells assessed as cell growth inhibition after 48 hrs by MTT assay Cytotoxicity against human MDA-MB-231 cells assessed as cell growth inhibition after 48 hrs by MTT assay	[PMID: 27363938]
MDA-MB-468	GI₅₀	17 μM Compound: 1	Cytotoxicity against human MDA-MB-468 cells assessed as cell growth inhibition after 48 hrs by MTT assay Cytotoxicity against human MDA-MB-468 cells assessed as cell growth inhibition after 48 hrs by MTT assay	[PMID: 27363938]
MIA PaCa-2	GI₅₀	19 μM Compound: 1	Cytotoxicity against human MIAPaCa2 cells assessed as cell growth inhibition after 48 hrs by MTT assay Cytotoxicity against human MIAPaCa2 cells assessed as cell growth inhibition after 48 hrs by MTT assay	[PMID: 27363938]
MIA PaCa-2	GI₅₀	19 μM Compound: 1	Growth inhibition of human MIAPaCa2 cells after 48 hrs by MTT assay Growth inhibition of human MIAPaCa2 cells after 48 hrs by MTT assay	[PMID: 29370702]
MOLT-4	GI₅₀	12 μM Compound: 1	Cytotoxicity against human MOLT4 cells assessed as cell growth inhibition after 48 hrs by MTT assay Cytotoxicity against human MOLT4 cells assessed as cell growth inhibition after 48 hrs by MTT assay	[PMID: 27363938]
NCI-H226	IC₅₀	>10 μM Compound: 5	Cytotoxicity against human NCI-H226 cells after 48 hrs by MTT assay Cytotoxicity against human NCI-H226 cells after 48 hrs by MTT assay	[PMID: 19757855]
PANC-1	GI₅₀	22 μM Compound: 1	Cytotoxicity against human PANC1 cells assessed as cell growth inhibition after 48 hrs by MTT assay Cytotoxicity against human PANC1 cells assessed as cell growth inhibition after 48 hrs by MTT assay	[PMID: 27363938]
PC-3	GI₅₀	19 μM Compound: 1	Cytotoxicity against human PC3 cells assessed as cell growth inhibition after 48 hrs by MTT assay Cytotoxicity against human PC3 cells assessed as cell growth inhibition after 48 hrs by MTT assay	[PMID: 27363938]
PC-3	GI₅₀	19 μM Compound: 1	Growth inhibition of human PC3 cells after 48 hrs by MTT assay Growth inhibition of human PC3 cells after 48 hrs by MTT assay	[PMID: 29370702]
PSN1	GI₅₀	23 μM Compound: 1	Cytotoxicity against human PSN1 cells assessed as cell growth inhibition after 48 hrs by MTT assay Cytotoxicity against human PSN1 cells assessed as cell growth inhibition after 48 hrs by MTT assay	[PMID: 27363938]
SF-295	GI₅₀	27 μM Compound: 1	Cytotoxicity against human SF295 cells assessed as cell growth inhibition after 48 hrs by MTT assay Cytotoxicity against human SF295 cells assessed as cell growth inhibition after 48 hrs by MTT assay	[PMID: 27363938]
SF-539	GI₅₀	30 μM Compound: 1	Cytotoxicity against human SF539 cells assessed as cell growth inhibition after 48 hrs by MTT assay Cytotoxicity against human SF539 cells assessed as cell growth inhibition after 48 hrs by MTT assay	[PMID: 27363938]
SNB-75	GI₅₀	22 μM Compound: 1	Cytotoxicity against human SNB75 cells assessed as cell growth inhibition after 48 hrs by MTT assay Cytotoxicity against human SNB75 cells assessed as cell growth inhibition after 48 hrs by MTT assay	[PMID: 27363938]
T47D	GI₅₀	24 μM Compound: 1	Cytotoxicity against human T47D cells assessed as cell growth inhibition after 48 hrs by MTT assay Cytotoxicity against human T47D cells assessed as cell growth inhibition after 48 hrs by MTT assay	[PMID: 27363938]
THP-1	GI₅₀	28 μM Compound: 1	Cytotoxicity against human THP1 cells assessed as cell growth inhibition after 48 hrs by MTT assay Cytotoxicity against human THP1 cells assessed as cell growth inhibition after 48 hrs by MTT assay	[PMID: 27363938]
U-251	GI₅₀	32 μM Compound: 1	Cytotoxicity against human U251 cells assessed as cell growth inhibition after 48 hrs by MTT assay Cytotoxicity against human U251 cells assessed as cell growth inhibition after 48 hrs by MTT assay	[PMID: 27363938]

In Vitro

Rohitukine (48 h) exhibits selective cytotoxicity against cancer cells, with the highest potency against HL-60 leukemia (GI₅₀ = 10 μM) and Molt-4 leukemia (GI₅₀ = 12 μM), and minimal cytotoxicity against normal fR2 and HEK-293 cell lines (GI₅₀ > 50 μM)^[1].
Rohitukine (1-10 μM) induces S-phase cell cycle arrest in HL-60 leukemia cells in a concentration-dependent manner^[1].
Rohitukine potently inhibits Cdk9/cyclin T1 (IC₅₀ = 0.3 μM) and weakly inhibits Cdk2/A (IC₅₀ = 7.3 μM) in cell-free biochemical assays^[1].
Rohitukine (50 μM) strongly inhibits Dyrk1A, AMPK, and VEGFR kinases in a cell-free profiling assay^[1].
Rohitukine (5-20 μM; 2-8 days) inhibits lipid accumulation in 3T3-L1 and C3H10T1/2 adipocytes in a concentration- and time-dependent manner^[2].
Rohitukine (20 μM; 48 h-6 days) downregulates pro-adipogenic gene expression (LPL, aP2, SREBP-1c, FAS, PPARγ) and upregulates anti-adipogenic gene expression (Wnt3a, GATA2) in 3T3-L1 adipocytes when treated with 20 μM for 6 days^[2].
Rohitukine (20 μM; 15 min-6 days) downregulates late-phase adipogenic protein expression (PPARγ, C/EBPα, aP2, FAS, GLUT4) and inhibits early AKT/mTOR/4EBP signaling in 3T3-L1 adipocytes^[2].
Rohitukine (1-20 μM; 24 h) arrests 3T3-L1 preadipocytes in S phase during mitotic clonal expansion in a concentration-dependent manner^[2].
Rohitukine (20 μM; 16-24 h) downregulates cell cycle progression proteins (cyclin-D, CDK6, CDK4, cyclin-E, CDK2, C/EBPβ) and stabilizes the CDK inhibitor P27 in 3T3-L1 preadipocytes^[2].
Rohitukine (20 μM; 48 h) significantly inhibits 3T3-L1 preadipocyte proliferation during mitotic clonal expansion^[2].
Rohitukine (3-100 μM; 24 h) exhibits no cytotoxicity toward J774A.1 macrophage cells, with a cytotoxic IC₅₀ >50 μM^[3].
Rohitukine (3-30 μM; 1 h pretreatment, followed by 18 h incubation) dose-dependently inhibits LPS (HY-D1056)-induced nitric oxide production in J774A.1 macrophage cells^[3].
Rohitukine (3-30 μM; 18 h) inhibits LPS-induced reactive oxygen species production in J774A.1 macrophage cells^[3].
Rohitukine (3-30 μM; 1 h pretreatment, followed by 18 h incubation) inhibits LPS-induced production of IL-1β, TNF-α, IL-6, and PGE₂ in J774A.1 macrophage cells^[3].
Rohitukine (3-30 μM; 1 h pretreatment, followed by 18 h incubation) dose-dependently inhibits LPS-induced NF-κB transcriptional activity in J774A.1 macrophage cells^[3].
Rohitukine (10-30 μM; 1 h pretreatment, followed by incubation) inhibits LPS-induced nuclear translocation of NF-κB in J774A.1 macrophage cells at concentrations of 10 and 30 μM^[3].
Rohitukine (10-30 μM; 1 h pretreatment, followed by 2 h incubation) suppresses LPS-induced iNOS and COX-2 protein expression in J774A.1 macrophage cells^[3].
Rohitukine (10-30 μM; 1 h pretreatment, followed by 30 min incubation) inhibits LPS-induced activation of the NF-κB pathway by reducing IκB-α phosphorylation and preserving cytosolic NF-κB p65, and inhibits LPS-induced activation of the MAPK pathway by reducing ERK and JNK phosphorylation in J774A.1 macrophage cells^[3].
Rohitukine (3-30 μM; 48 h) is non-toxic to primary murine peritoneal macrophages up to 50 μM, and dose-dependently inhibits LPS-induced NO production and release of IL-1β, IL-6, and TNF-α^[3].
Rohitukine (0.25-1.0 mM) dose-dependently inhibits growth of five-week-old wild-type Arabidopsis thaliana (Col-0) plants^[4].
Rohitukine (0.25-1.0 mM) dose-dependently induces ROS accumulation and increases antioxidant enzyme activity in five-week-old wild-type Arabidopsis thaliana (Col-0) plants^[4].

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

Cell Differentiation Assay^[2]

Cell Line:

3T3-L1, C3H10T1/2 adipocytes
Concentration:

5; 10; 15; 20 μM
Incubation Time:

2; 4; 6; 8 days
Result:

Inhibited lipid accumulation in a concentration-dependent manner.
Significantly reduced lipid accumulation at 5 μM.
Inhibited >80% of MDI-induced lipid accumulation at 20 μM in both cell lines.
Reduced lipid accumulation across all time windows of 20 μM exposure, with maximum inhibition seen with 0-6 days exposure.
Caused a significant reduction in lipid accumulation in 3T3-L1 cells with the shortest 0-2 days exposure.

Real Time qPCR^[2]

Cell Line:

3T3-L1 adipocytes
Concentration:

20 μM
Incubation Time:

6 days (gene expression); 48 h (Wnt3a/GATA2 expression)
Result:

Significantly reduced mRNA expression of pro-adipogenic genes LPL, aP2, SREBP-1c, FAS, and PPARγ.
Caused a nonsignificant decreasing trend in C/EBPα mRNA expression.
Increased mRNA expression of anti-adipogenic transcription factors Wnt3a and GATA2 significantly after 48 h of exposure.

Western Blot Analysis^[2]

Cell Line:

3T3-L1 adipocytes
Concentration:

20 μM
Incubation Time:

15; 30; 60; 120 min; 2; 4; 6; days
Result:

Significantly suppressed late-phase protein expression of PPARγ, C/EBPα, aP2, FAS, and GLUT4 on days 2, 4, and 6 of differentiation.
Significantly reduced phosphorylation of AKT (Ser473), mTOR (Ser2448), and 4EBP (Thr37/46) within 2 hours of induction.

Cell Cycle Analysis^[2]

Cell Line:

3T3-L1 preadipocytes
Concentration:

1; 3; 10; 20 μM
Incubation Time:

24 hours
Result:

Caused a concentration-dependent increase in the percentage of cells in S phase.
Induced S-phase arrest during mitotic clonal expansion, with 41.15% of cells in S phase at 20 μM, compared to 19.28% in MDI-only treated cells.

Western Blot Analysis^[2]

Cell Line:

3T3-L1 preadipocytes
Concentration:

20 μM
Incubation Time:

16; 24 h
Result:

Reduced protein expression of cyclin-D, CDK6, CDK4, cyclin-E, CDK2, and C/EBPβ at 16 and 24 hours post-induction.
Stabilized expression of the CDK inhibitor P27.

Cell Viability Assay^[3]

Cell Line:

J774A.1 macrophage cells
Concentration:

3; 10; 30; 100 μM
Incubation Time:

24 h
Result:

Showed no cytotoxic effects across all tested concentrations, with cell viability remaining near control levels both with and without LPS co-treatment.
Determined a cytotoxic IC₅₀ >50 μM.

ELISA Assay^[3]

Cell Line:

J774A.1 macrophage cells
Concentration:

3; 10; 30 μM
Incubation Time:

1 h pretreatment, followed by 18 h incubation
Result:

Inhibited LPS-induced release of IL-1β (46%), TNF-α (29%), IL-6 (31%), and PGE₂ (48%) at 30 μM compared to the LPS-only control.
Showed inhibitory effects at lower concentrations in a dose-dependent manner.

Immunofluorescence^[3]

Cell Line:

J774A.1 macrophage cells
Concentration:

10; 30 μM
Incubation Time:

1 h pretreatment
Result:

Significantly reduced LPS-induced nuclear translocation of NF-κB, as measured by decreased fluorescent intensity of nuclear NF-κB.
Showed statistically significant inhibition at both 10 μM and 30 μM compared to the LPS-only group.

Western Blot Analysis^[3]

Cell Line:

J774A.1 macrophage cells
Concentration:

10; 30 μM
Incubation Time:

1 h pretreatment, followed by 2 h incubation
Result:

Reduced LPS-induced iNOS and COX-2 protein levels by 54% and 68%, respectively, at 30 μM.
Produced significant inhibitory effects on both proteins at 10 μM.

Western Blot Analysis^[3]

Cell Line:

J774A.1 macrophage cells
Concentration:

10; 30 μM
Incubation Time:

1 h pretreatment, followed by 30 min incubation
Result:

Downregulated LPS-induced phosphorylation of IκB-α.
Reduced LPS-induced depletion of cytosolic NF-κB p65.
Inhibited LPS-induced phosphorylation of ERK (27% inhibition at 30 μM) and JNK (54% inhibition at 30 μM).

Parmacokinetics

Species	Dose	Route	C_max	AUC_0-∞	MRT	T_max	Bioavailability
Golden hamster^[2]	50 mg/kg	p.o.	6.62 μg/mL	10.66 μg·h/mL	6.64 h	0.25 h	25.7 %
Golden hamster^[2]	5 mg/kg	i.v.	5.37 μg/mL	4.14 μg·h/mL	7.07 h	/	/

In Vivo

Rohitukine (50 mg/kg; p.o.; once daily; 7 days) significantly ameliorates high-fat diet-induced dyslipidemia in Syrian golden hamsters, reduces hepatic and gonadal lipid accumulation, and modulates key lipid-regulating genes and proteins^[2].
Rohitukine (12.5-50 mg/kg; p.o.; daily; 5 days) dose-dependently inhibits LPS-induced pro-inflammatory cytokine production in mice^[3].
Rohitukine (12.5-50 mg/kg; p.o.; single dose) dose-dependently reduces Acetic Acid (HY-Y0319)-induced vascular permeability in mice^[3].
Rohitukine (12.5-50 mg/kg; p.o.; single dose) dose-dependently inhibits Carrageenan (HY-125474)-induced paw oedema in rats^[3].
Rohitukine (12.5-50 mg/kg; p.o.; single dose) inhibits Carrageenan-induced pleurisy in mice^[3].
Rohitukine (12.5-50 mg/kg; p.o.; daily; 14 days) dose-dependently reduces Freund's complete adjuvant-induced arthritis in rats^[3].

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

Animal Model:

Syrian golden hamster (8-week-old, 100-120 g body weight, dyslipidemia induced by 45% kcal high-fat diet for 10 days)^[2]
Dosage:

50 mg/kg
Administration:

p.o.; once daily; 7 days
Result:

Reduced body weight gain significantly compared to HFD and pair-fed groups.
Reduced plasma total cholesterol, triglycerides, LDL-cholesterol, and HDL-cholesterol levels significantly relative to the pair-fed group.
Increased HDL-cholesterol/total cholesterol ratio significantly.
Increased hepatic mRNA expression of liver X receptor α 4-fold.
Reduced LDL receptor, HMG-CoA reductase, and sterol-regulatory element binding protein 2 expression significantly.
Decreased epididymal adipose tissue weight significantly compared to HFD-fed animals.
Reduced protein expression of peroxisome proliferator-activated receptor γ, fatty acid synthase, adipocyte protein 2, and glucose transporter 4 in epididymal adipose tissue.
Reduced lipid accumulation in liver, smaller adipocyte size, and reduced pancreatic lipid droplets compared to HFD-fed hamsters.

Animal Model:

BALB/c mice (male, 22-25 g, LPS-induced pro-inflammatory cytokine production model)^[3]
Dosage:

12.5; 25; 50 mg/kg
Administration:

p.o.; daily; 5 days
Result:

Inhibited LPS-induced IL-1β production by 58%, TNF-α production by 45%, and IL-6 production by 38% at 50 mg/kg.
Significantly reduced IL-1β and TNF-α levels at 25 mg/kg.
Reduced IL-1β, TNF-α, and IL-6 levels compared to the LPS-only group at 12.5 mg/kg.

Animal Model:

BALB/c mice (male, 22-25 g, acetic acid-induced vascular permeability model)^[3]
Dosage:

12.5; 25; 50 mg/kg
Administration:

p.o.; single dose
Result:

Reduced Evans blue leakage by 12.1% at 12.5 mg/kg, 39.3% at 25 mg/kg, and 75.7% at 50 mg/kg compared to the acetic acid control group.

Animal Model:

Wistar rats (male, 120-140 g, Carrageenan (HY-125474)-induced paw oedema model)^[3]
Dosage:

12.5; 25; 50 mg/kg
Administration:

p.o.; single dose
Result:

Suppressed paw oedema by 25% at 12.5 mg/kg, 35% at 25 mg/kg, and 58% at 50 mg/kg compared to the carrageenan control group.

Animal Model:

BALB/c mice (male, 22-25 g, carrageenan-induced pleurisy model)^[3]
Dosage:

12.5; 25; 50 mg/kg
Administration:

p.o.; single dose
Result:

Inhibited pleuritic exudate volume by 59.95% and total leukocyte migration by 86.04% at 50 mg/kg.
Inhibited exudate volume by 61.43% and leukocyte migration by 82.43% at 25 mg/kg.
Inhibited exudate volume by 5.90% and leukocyte migration by 36.82% at 12.5 mg/kg.

Animal Model:

Wistar rats (male, 120-140 g, Freund's complete adjuvant-induced arthritis model)^[3]
Dosage:

12.5; 25; 50 mg/kg
Administration:

p.o.; daily; 14 days
Result:

Inhibited paw oedema by 54%, reduced TNF-α levels by 52%, IL-6 levels by 68%, and IL-1β levels by 71% compared to the arthritic disease control group at 50 mg/kg.
Restored serum SGPT, creatinine, and triglyceride levels to near normal at 50 mg/kg.
Augmented serum SOD, CAT, and GST levels by 96%, 94%, and 98% respectively compared to the arthritic group at 50 mg/kg.
Improved spontaneous motor activity to 39.90 at 50 mg/kg.
Maintained joint architecture with reduced bone erosion on radiographs at 50 mg/kg.
Prevented body weight loss in all treated groups.

Chemical Information

CAS No. 71294-60-5
분자량 305.33
화학식 C₁₆H₁₉NO₅
SMILES

O=C1C=C(OC2=C1C(O)=CC(O)=C2[C@@H]3[C@@H](CN(CC3)C)O)C
선적

Room temperature in continental US; may vary elsewhere.
보관

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

순도&문서

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (298 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]. Kumar V, et al. A chromatography-free isolation of rohitukine from leaves of Dysoxylum binectariferum: Evaluation for in vitro cytotoxicity, Cdk inhibition and physicochemical properties. Bioorg Med Chem Lett. 2016 Aug 1;26(15):3457-63. [Content Brief]

[2]. Varshney S, et al. Rohitukine inhibits in vitro adipogenesis arresting mitotic clonal expansion and improves dyslipidemia in vivo. J Lipid Res. 2014 Jun;55(6):1019-32. [Content Brief]

[3]. Singh A, et al. Rohitukine inhibits NF-κB activation induced by LPS and other inflammatory agents. Int Immunopharmacol. 2019 Apr;69:34-49. [Content Brief]

[4]. Ahmed S, et al. Exogenously Applied Rohitukine Inhibits Photosynthetic Processes, Growth and Induces Antioxidant Defense System in Arabidopsis thaliana. Antioxidants (Basel). 2022 Aug 3;11(8):1512. [Content Brief]

[5]. Kumara PM, et al. Rohitukine, a chromone alkaloid and a precursor of flavopiridol, is produced by endophytic fungi isolated from Dysoxylum binectariferum Hook.f and Amoora rohituka (Roxb).Wight & Arn. Phytomedicine. 2014 Mar 15;21(4):541-6. [Content Brief]

[6]. Houghton PJ, et al. Further Chromone Alkaloids from Schumanniophyton magnificum. Planta Med. 1987 Jun;53(3):262-4. [Content Brief]

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Rohitukine

All NF-κB Isoforms

All CDK Isoforms

All PPAR Isoforms

All Akt Isoforms

All mTOR Isoforms

All Wnt Isoforms

All Interleukin Related Isoforms

All p38 MAPK Isoforms

All ERK Isoforms

All JNK Isoforms

Biological Activity

Chemical Information

순도&문서

References

Calculators

Help & FAQs

Rohitukine Related Classifications

HY-119831 Related Classifications