Cat. No.: HY-N0559

Kirenol

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Kirenol is a diterpenoid compound, an orally active apoptosis inducer and signaling pathway regulator, with a K_d value of 5.47 μM against the target CK2. Kirenol promotes the cleavage of Bid into tBid, regulates the protein levels/phosphorylation of Bax, Bcl-2, p53 and p21, and induces caspase-independent apoptosis, S-phase cell cycle arrest, ROS accumulation and cytotoxicity in cancer cells. Kirenol activates the CK2/AKT and AMPK-mTOR-ULK1 pathways, inhibits the signaling of NF-κB, TGF-β/Smads and NLRP3 inflammasome, and regulates the GSK3β, BMP and Wnt/β-catenin pathways. Kirenol induces autophagy, mitophagy and osteoblast differentiation, promotes mitochondrial fusion, and exerts antioxidant, anti-inflammatory, antifibrotic, renoprotective, cardioprotective, neuroprotective and analgesic effects. Kirenol is applicable to research related to chronic myeloid leukemia, ischemic stroke, diabetic nephropathy, heart failure, acute lung injury and osteoporosis.

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Pureté: 99.82%
CAS No.: 52659-56-0
Formule: C₂₀H₃₄O₄
Masse moléculaire:338.48

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-20°C, protect from light

* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Kirenol Chemical Structure

CAS No.: 52659-56-0

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Activité biologique
- Description
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Publications (1)
Solvant et solubilité
- In Vitro
- In Vivo
Pureté et documentation
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Activité biologique

Description

Voir tous les produits spécifiques à Isoform Casein Kinase :

Voir tous les produits spécifiques à Isoform AMPK :

Voir tous les produits spécifiques à Isoform Akt :

Voir tous les produits spécifiques à Isoform NF-κB :

Voir tous les produits spécifiques à Isoform TGF-beta/Smad :

Smad1
Smad3

Cellular Effect

Cell Line	Type	Value	Description	References
B16	IC₅₀	>100 μg/mL Compound: 5	Cytotoxicity against mouse B16 cells after 44 hrs by MTT assay Cytotoxicity against mouse B16 cells after 44 hrs by MTT assay	[PMID: 19928884]
HSC-T6	IC₅₀	>100 μg/mL Compound: 5	Cytotoxicity against rat HSC-T6 cells after 44 hrs by MTT assay Cytotoxicity against rat HSC-T6 cells after 44 hrs by MTT assay	[PMID: 19928884]
MDA-MB-231	IC₅₀	>10 μM Compound: 19	Antiinvasive activity in human MDA-MB-231 cells assessed as inhibition of EGF-induced cell invasion after 3.5 hrs Antiinvasive activity in human MDA-MB-231 cells assessed as inhibition of EGF-induced cell invasion after 3.5 hrs	[PMID: 28009521]
RAW264.7	IC₅₀	>100 μM Compound: 19	Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced nitric oxide production after 24 hrs by Griess assay Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced nitric oxide production after 24 hrs by Griess assay	[PMID: 28009521]

In Vitro

Kirenol (10-40 μg/mL; 24-72 h) potently inhibits proliferation of human chronic myeloid leukemia K562 cells in a time- and dose-dependent manner, with IC₅₀ values of 53.05 μg/mL (24 h), 18.19 μg/mL (48 h), and 15.08 μg/mL (72 h)^[1].
Kirenol (10-40 μg/mL; 24 h) induces dose-dependent apoptosis in human chronic myeloid leukemia K562 cells, with apoptosis rates ranging from 8.29% to 51.85%^[1].
Kirenol (40 μg/mL; 12-48 h) induces time-dependent loss of mitochondrial membrane potential in human chronic myeloid leukemia K562 cells over 12, 24, and 48 h^[1].
Kirenol (40 μg/mL; 12-48 h) induces time-dependent accumulation of ROS in human chronic myeloid leukemia K562 cells over 12, 24, and 48 h^[1].
Kirenol (40 μg/mL; 12-48 h) modulates Bcl-2 family protein expression in human chronic myeloid leukemia K562 cells, reducing Bcl-2 levels and increasing Bax and tBid levels over 12, 24, and 48 h, and upregulating phosphorylation of p53 (Ser 6 and Ser 37) and p21 protein expression^[1].
Kirenol (10-40 μg/mL; 48 h) induces dose-dependent S-phase cell cycle arrest in human chronic myeloid leukemia K562 cells^[1].
Kirenol (1.25-5% Kirenol-containing serum; 24 h (prior to TBHP treatment)) exerts anti-apoptotic and antioxidant effects in TBHP-injured HT22 cells by modulating apoptotic proteins, reducing ROS, and restoring antioxidant/oxidative stress marker balance^[2].
Kirenol (1.25-5% Kirenol-containing serum; 24 h (prior to TBHP treatment)) preserves mitochondrial function and promotes Opa1-mediated mitochondrial fusion in TBHP-injured HT22 cells, reversing fragmentation, increasing ATP production, restoring MMP, and upregulating Opa1 expression^[2].
Kirenol (10-80 μM pre-incubated 30 min then co-treated with 30 mM glucose for 24 h; 20 μM pre-incubated 30 min then co-treated with 10 ng/mL TGF-β1 for 24 h) inhibits activation of the TGF-β/Smads pathway and reduces extracellular matrix protein accumulation in primary mouse mesangial cells^[3].
Kirenol (20 μM; 3 h pre-incubation prior to 24 h Ang II stimulation) suppresses Ang II-induced NLRP3 inflammasome activation and mitochondrial ROS production in mouse bone marrow-derived macrophages by enhancing mitophagy, as these effects are reversed by mitophagy inhibition^[4].
Kirenol (50-200 μg/mL; 24 h post-LPS challenge) dose-dependently inhibits TNF-α mRNA expression in LPS-challenged A549 cells^[6].
Kirenol (50-200 μg/mL; 24 h post-LPS challenge) dose-dependently enhances autophagy in LPS-challenged A549 cells, as shown by increased LC3-II and decreased p62 protein levels^[6].
Kirenol (200 μg/mL; 24 h post-LPS challenge) activates the AMPK-mTOR-ULK1 pathway in LPS-challenged A549 cells, as shown by increased p-AMPK and p-ULK1, and decreased p-mTOR protein levels^[6].
Kirenol (10-40 μM; 3 days) dose-dependently upregulates the mRNA expression of key osteoblast differentiation markers (ALP, ColA1, OPN) in MC3T3-E1 cells, with significant increases of 67.8%, 40.0%, and 67.7% respectively at 40 μM after 3 days of treatment^[7].
Kirenol (10-40 μM; 3 days) dose-dependently activates the BMP signaling pathway in MC3T3-E1 cells after 3 days of treatment at 10, 20, and 40 μM by upregulating the mRNA expression of BMP2, Runx2, and Osx^[7].

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

Apoptosis Analysis^[1]

Cell Line:

human chronic myeloid leukemia K562 cells
Concentration:

40 μg/mL
Incubation Time:

24 h
Result:

Induced marked nuclear condensation and fragmentation in K562 cells, as indicated by fluorescent staining.

Western Blot Analysis^[1]

Cell Line:

human chronic myeloid leukemia K562 cells
Concentration:

40 μg/mL
Incubation Time:

12, 24, 48 h
Result:

Caused a significant decrease in mitochondrial cytochrome c levels at 12 and 24 h. Induced a marked increase in cytosolic cytochrome c levels at 24 h.
Decreased Bcl-2 protein levels at 24 and 48 h. Upregulated Bax and tBid (cleaved Bid) protein levels at 12, 24, and 48 h.\nIncreased phosphorylation of p53 at Ser 6 and Ser 37 at 24 and 48 h, with no change in total p53 levels. Significantly increased p21 protein levels at 12, 24, and 48 h.

Cell Cycle Analysis^[1]

Cell Line:

human chronic myeloid leukemia K562 cells
Concentration:

10-40 μg/mL
Incubation Time:

48 h
Result:

Induced dose-dependent S-phase cell cycle arrest, with S-phase population increasing from 48.99% (untreated) to 52.89% (10 μg/mL), 56.05% (20 μg/mL), and 70.04% (40 μg/mL).

Western Blot Analysis^[3]

Cell Line:

Primary mouse mesangial cells
Concentration:

10-80 μM
Incubation Time:

24 h (co-treatment); 30 min (pre-incubation)
Result:

Reduced high glucose-induced increases in fibronectin and collagen IV levels. Inhibited high glucose-induced phosphorylation of Smad2/3. Suppressed TGF-β1-induced phosphorylation of Smad2/3. Attenuated TGF-β1-induced increases in fibronectin and collagen IV levels. Did not alter baseline levels of these proteins when treated alone at 20 μM.

Real Time qPCR^[6]

Cell Line:

A549 (LPS-challenged acute lung injury cell model)
Concentration:

50-200 μg/mL
Incubation Time:

1 h pre-incubation, then 24 h with LPS
Result:

Dose-dependently reduced LPS-induced TNF-α mRNA expression.

Immunofluorescence^[6]

Cell Line:

A549 (LPS-challenged acute lung injury cell model)
Concentration:

200 μg/mL
Incubation Time:

1 h pre-incubation, then 24 h with LPS
Result:

Increased the number of LC3 dots per cell relative to LPS-only treated cells.
Decreased p62 fluorescence intensity per cell relative to LPS-only treated cells.
Decreased mTOR fluorescence intensity per cell relative to LPS-only treated cells.
Decreased p-mTOR fluorescence intensity per cell relative to LPS-only treated cells.

Cell Viability Assay^[7]

Cell Line:

MC3T3-E1 pre-osteoblastic cells
Concentration:

10-40 μM
Incubation Time:

24 h
Result:

Showed no significant cytotoxicity at 10, 20, and 40 μM.

RT-PCR^[7]

Cell Line:

MC3T3-E1 pre-osteoblastic cells undergoing osteoblast differentiation
Concentration:

10-40 μM
Incubation Time:

3 days
Result:

Increased mRNA expression of ALP, type I collagen (ColA1), and osteopontin (OPN) in a dose-dependent manner; increased ALP mRNA expression by 67.8%, ColA1 by 40.0%, and OPN by 67.7% at 40 μM compared to control.
Increased mRNA expression of osteoprotegerin (OPG), while decreased receptor activator of nuclear factor kappa B ligand (RANKL) mRNA expression, resulting in an increased OPG/RANKL ratio.\nSignificantly increased mRNA expression of BMP2, runt-related transcription factor 2 (Runx2), and osterix (Osx) in a dose-dependent manner.
Significantly increased mRNA expression of low density lipoprotein receptor related protein 5 (LRP5), disheveled 2 (DVL2), β-catenin, and cyclin D1 (CCND1) in a dose-dependent manner.

In Vivo

Kirenol (1.25-5 mg/kg; i.p.; daily; 7 days) exerts dose-dependent neuroprotective effects in MCAO/R rats, reducing cerebral infarct volume by up to ~55% at 5 mg/kg, improving neurological function, mitigating oxidative stress, and promoting Opa1-mediated mitochondrial fusion via activation of the CK2/AKT pathway^[2].
Kirenol (2 mg/kg; p.o.; daily; 3 months) alleviates diabetic nephropathy in male C57BL/6J mice by reducing phosphorylation of Smad2/3 (0.64-fold) and NF-κB (0.43-fold), restoring IκBα levels, decreasing ECM accumulation and inflammatory cytokine expression, and improving renal structural and functional markers^[3].
Kirenol (50 mg/kg; i.p.; daily; starting 1 day pre-surgery until study end) exerts cardioprotective effects in pressure overload-induced heart failure by improving cardiac function, reducing hypertrophy and fibrosis, suppressing inflammatory responses, and enhancing macrophage mitophagy, with these benefits abrogated by mitophagy inhibition^[4].
Kirenol (0.1-0.5% (w/w); topical; single application of 0.3 g cream) dose-dependently inhibits carrageenan-induced acute paw edema and reduces local pro-inflammatory cytokine (IL-1β, TNF-α) levels^[5].
Kirenol (100 mg/kg; i.p.; daily; 7 days) significantly reduces LPS-induced acute lung injury in Balb/c mice by enhancing autophagy and inhibiting inflammation, as evidenced by reduced inflammatory cytokine levels, improved lung histopathology, and decreased lung edema and leukocyte infiltration^[6].

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

Animal Model:

Sprague-Dawley (male, 200-240 g, ischemic stroke model via MCAO/R)^[2]
Dosage:

1.25 mg/kg; 2.5 mg/kg; 5 mg/kg
Administration:

i.p.; daily; 7 days
Result:

Significantly reduced modified Neurological Severity Scores (mNSS), increased paw grip tension, and reduced right turn frequency on days 5 and 7 post-treatment.
Significantly reduced cerebral infarct volume, with the 5 mg/kg group showing reduction to ~18% infarct volume (vs ~40% in MCAO controls), corresponding to up to ~55% reduction.
Reduced neuronal nuclear contraction and cell spacing in the ischemic cortex, with improved cell structure organization.
Significantly increased levels of superoxide dismutase (SOD), glutathione (GSH), glutathione peroxidase (GPx), and SOD2 protein expression, while significantly reducing levels of malondialdehyde (MDA) and lactate dehydrogenase (LDH) in peri-infarct brain tissue.\nSignificantly increased optic atrophy 1 (Opa1) protein expression without altering levels of Fis1, Drp1, MFN1, MFN2.\nSignificantly increased CK2 protein levels and AKT phosphorylation (p-AKT/AKT ratio) in peri-infarct brain tissue.

Animal Model:

C57BL/6J (male, ~20 g, diabetic nephropathy induced via 2 months high-fat diet + 5 consecutive days 100 mg/kg streptozotocin i.p. injection)^[3]
Dosage:

2 mg/kg
Administration:

p.o.; daily; 3 months
Result:

Did not lower blood glucose but improved the kidney/body weight ratio.
Ameliorated serum creatinine and blood urea nitrogen levels.
Alleviated diabetes-induced mesangial expansion, focal interstitial inflammation, glomerular atrophy, and glomerular sclerosis.
Reduced glomerular basement membrane thickness and podocyte foot process fusion.
Decreased phosphorylation of Smad2/3 by 0.64-fold, and reduced accumulation of fibronectin (FN) and collagen IV (Col IV) by 0.58-fold and 0.35-fold, respectively.
Restored IκBα expression to normal levels.
Decreased phosphorylation of NF-κB by 0.43-fold.
Reduced IL-6 and TNF-α expression by 0.57-fold and 0.46-fold, respectively.
Reduced FN-positive area and collagen fiber accumulation in renal tissue.

Animal Model:

C57BL/6J (8-week-old male)^[4]
Dosage:

50 mg/kg
Administration:

i.p.; daily; starting 1 day pre-surgery until study end
Result:

Increased left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) compared to vehicle-treated TAC mice.
Reduced end-diastolic left ventricular internal dimension (LVIDd) compared to vehicle-treated TAC mice.
Reduced mRNA levels of cardiac stress biomarkers ANP and BNP compared to vehicle-treated TAC mice.
Lowered heart weight to body weight (HW/BW) ratios compared to vehicle-treated TAC mice.
Decreased cardiomyocyte cross-sectional area compared to vehicle-treated TAC mice.
Reduced cardiac collagen deposition (fibrosis) measured by Masson's trichrome staining compared to vehicle-treated TAC mice.
Lowered mRNA expression of fibrosis markers α-SMA, COL1, and COL3 compared to vehicle-treated TAC mice.
Decreased cardiac infiltration of CD11b⁺F4/80⁺ macrophages compared to vehicle-treated TAC mice.
Reduced NLRP3 protein expression in heart tissue compared to vehicle-treated TAC mice.
Lowered serum levels of pro-inflammatory cytokines TNF-α, IL-6, IL-18, and IL-1β compared to vehicle-treated TAC mice.

Animal Model:

Wistar rats (male, SPF, 250-300 g)^[5]
Dosage:

0.1% (w/w); 0.2% (w/w); 0.3% (w/w); 0.4% (w/w); 0.5% (w/w)
Administration:

topical; single application of 0.3 g cream
Result:

Produced 36.87%, 40.02%, 39.01%, and 42.62% reduction in paw edema at 1, 2, 3, and 4 hours post-carrageenan injection, respectively, with statistically significant differences vs. base cream at all time points.
Produced 48.88%, 43.01%, 42.77%, and 47.20% reduction in paw edema at 1, 2, 3, and 4 hours post-carrageenan injection, respectively, with statistically significant differences vs. base cream at all time points.
Produced 57.28%, 55.34%, 46.21%, and 48.90% reduction in paw edema at 1, 2, 3, and 4 hours post-carrageenan injection, respectively, with statistically significant differences vs. base cream.
Produced 65.37%, 65.21%, 61.25%, and 64.21% reduction in paw edema at 1, 2, 3, and 4 hours post-carrageenan injection, respectively, with statistically significant differences vs. base cream; this anti-inflammatory effect was similar to that of 0.5% piroxicam gel at 4 hours post-carrageenan injection.
Produced 81.09%, 74.82%, 76.31%, and 76.78% reduction in paw edema at 1, 2, 3, and 4 hours post-carrageenan injection, respectively, with statistically significant differences vs. base cream; this anti-inflammatory effect was similar to that of 0.5% piroxicam gel at 4 hours post-carrageenan injection.
Significantly reduced carrageenan-induced increases in IL-1β and TNF-α levels in subcutaneous plantar tissue.

Animal Model:

Balb/c (6-8 weeks old, 18-22 g, 20 female, 20 male, LPS-induced ALI)^[6]
Dosage:

100 mg/kg
Administration:

i.p.; daily; 7 consecutive days
Result:

Significantly decreased LPS-induced serum levels of IL-1β, IL-6, and TNF-α.
Significantly decreased LPS-induced lung homogenate levels of IL-1β, IL-6, and TNF-α.
Increased lung tissue LC3-II protein expression and decreased lung tissue p62 protein expression compared to LPS-only mice.
Attenuated LPS-induced lung pathological injuries (including alveolar collapse, stromal hemorrhage, pulmonary edema, and inflammatory cell infiltration).
Reduced lung wet/dry weight ratio, decreased bronchoalveolar lavage fluid (BALF) protein concentration, reduced total BALF cell count, lowered BALF neutrophil percentage, and decreased lung myeloperoxidase (MPO) activity compared to LPS-only mice.

Chemical Information

CAS No. 52659-56-0
Appearance Solid
Masse moléculaire 338.48
Formule C₂₀H₃₄O₄
Color Off-white to light yellow
SMILES

C[C@]([C@@](CC1)([H])[C@]2(C)CO)(C[C@H](O)C2)[C@@]3([H])C1=C[C@]([C@@H](O)CO)(C)CC3
Structure Classification
- Terpenoids
- Diterpenoids
Initial Source
- Plants
- Compositae
Livraison

Room temperature in continental US; may vary elsewhere.
Stockage

-20°C, protect from light

* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Publications (1)

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Int J Cardiol

Kirenol attenuates pressure overload-induced heart failure by enhancing autophagy in macrophages. [Abstract]

2025 Dec 1:440:133681. PMID: 40752803

Solvant et solubilité

In Vitro:

DMSO : 100 mg/mL (295.44 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

H₂O : < 0.1 mg/mL (insoluble)

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Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

2.9544 mL

14.7719 mL

29.5438 mL

5 mM

0.5909 mL

2.9544 mL

5.9088 mL

10 mM

0.2954 mL

1.4772 mL

2.9544 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 (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

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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:
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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: ≥ 3.25 mg/mL (9.60 mM); Clear solution

This protocol yields a clear solution of ≥ 3.25 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (32.5 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: ≥ 3.25 mg/mL (9.60 mM); Clear solution

This protocol yields a clear solution of ≥ 3.25 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (32.5 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: ≥ 3.25 mg/mL (9.60 mM); Clear solution

This protocol yields a clear solution of ≥ 3.25 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 (32.5 mg/mL) to 900 μL Corn oil, and mix evenly.

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Working solution concentration: 0.22 mg/mL

Pureté et documentation

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Pureté: 99.98%

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ee.: 99.98%

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Références

[1]. Lu Y, et al. Kirenol, a compound from Herba Siegesbeckiae, induces apoptosis in human chronic myeloid leukemia K562 cells. Pharmazie. 2014;69(2):148-153. [Content Brief]

[2]. Zhang Y, et al. Kirenol alleviates cerebral ischemia-reperfusion injury by reducing oxidative stress and ameliorating mitochondrial dysfunction via activating the CK2/AKT pathway. Free Radic Biol Med. 2025;232:353-366. [Content Brief]

[3]. Li J, et al. Kirenol alleviates diabetic nephropathy via regulating TGF-β/Smads and the NF-κB signal pathway. Pharm Biol. 2022;60(1):1690-1700. [Content Brief]

[4]. Huang Z, et al. Kirenol attenuates pressure overload-induced heart failure by enhancing autophagy in macrophages. Int J Cardiol. 2025;440:133681. [Content Brief]

[5]. Wang JP, et al. Topical anti-inflammatory and analgesic activity of kirenol isolated from Siegesbeckia orientalis. J Ethnopharmacol. 2011;137(3):1089-1094. [Content Brief]

[6]. Xiao J, et al. Kirenol inhibits inflammation challenged by lipopolysaccharide through the AMPK-mTOR-ULK1 autophagy pathway. Int Immunopharmacol. 2023;116:109734. [Content Brief]

[7]. Kim MB, et al. Kirenol stimulates osteoblast differentiation through activation of the BMP and Wnt/β-catenin signaling pathways in MC3T3-E1 cells. Fitoterapia. 2014;98:59-65. [Content Brief]

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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
DMSO	1 mM	2.9544 mL	14.7719 mL	29.5438 mL	73.8596 mL
	5 mM	0.5909 mL	2.9544 mL	5.9088 mL	14.7719 mL
	10 mM	0.2954 mL	1.4772 mL	2.9544 mL	7.3860 mL
	15 mM	0.1970 mL	0.9848 mL	1.9696 mL	4.9240 mL
	20 mM	0.1477 mL	0.7386 mL	1.4772 mL	3.6930 mL
	25 mM	0.1182 mL	0.5909 mL	1.1818 mL	2.9544 mL
	30 mM	0.0985 mL	0.4924 mL	0.9848 mL	2.4620 mL
	40 mM	0.0739 mL	0.3693 mL	0.7386 mL	1.8465 mL
	50 mM	0.0591 mL	0.2954 mL	0.5909 mL	1.4772 mL
	60 mM	0.0492 mL	0.2462 mL	0.4924 mL	1.2310 mL
	80 mM	0.0369 mL	0.1846 mL	0.3693 mL	0.9232 mL
	100 mM	0.0295 mL	0.1477 mL	0.2954 mL	0.7386 mL

Kirenol

1 Cited Publications

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Kirenol

Apoptosis Compound Library

Cell Cycle/DNA Damage Compound Library

Epigenetics Compound Library

Immunology/Inflammation Compound Library

Kinase Inhibitor Library

NF-κB Signaling Compound Library

PI3K/Akt/mTOR Compound Library

Stem Cell Signaling Compound Library

TGF-beta/Smad Compound Library

Wnt/Hedgehog/Notch Compound Library

Natural Product Library

Anti-Cancer Compound Library

Autophagy Compound Library

Anti-Aging Compound Library

Antioxidant Compound Library

Differentiation Inducing Compound Library

Anti-diabetic Compound Library

Oxygen Sensing Compound Library

Anti-Cardiovascular Disease Compound Library

Terpenoids Library

Glycolysis Compound Library

Pyroptosis Compound Library

Cytoskeleton Compound Library

Glutamine Metabolism Compound Library

Traditional Chinese Medicine Active Compound Library

Neuroprotective Compound Library

Anti-Breast Cancer Compound Library

Anti-Lung Cancer Compound Library

Anti-Pancreatic Cancer Compound Library

Anti-Blood Cancer Compound Library

Anti-Cancer Metabolism Compound Library

Anti-Obesity Compound Library

Angiogenesis-Related Compound Library

Transcription Factor-Targeted Library

Lipid Metabolism Compound Library

Glucose Metabolism Compound Library

Anti-Liver Cancer Compound Library

Anti-Colorectal Cancer Compound Library

Anti-Cancer Natural Product Library

Antidepressant Compound Library

Anti-inflammatory Traditional Chinese Medicine Active Compound Library

Plant-Sourced Natural Product Library

Human Metabolite Library

Anti-Prostate Cancer Compound Library

Anti-Pulmonary Fibrosis Compound Library

Osteogenesis Compound Library

Cancer Stem Cells Compound Library

Pain-Related Compound Library

Cell Death Library

Serine/Threonine Kinase Inhibitor Library

Anti-Hematopathy Compound Library

Anti-Ovarian Cancer Compound Library

Inflammasomes related Compound Library

Multi-Target Compound Library

Radioprotector Library

Mitophagy Compound Library

Bioactive Compound Library Max

MCE Bioactive Compound Library

Natural Product Library Plus

Natural Product and Natural Product-Like Compound Library

Bioactive Compound Library

Anti-Gastric Cancer Compound Library

Anti-Fibrosis Compound Library

Protein Kinase Compound Library

Non-Alcoholic Fatty Liver Disease (NAFLD) Compound Library

RO5 Drug-like Natural Product Library

Cell Proliferation Compound Library

Lactic Acid Metabolic Compound Library

High-Throughput Bioactive Compound Library

High-Throughput Natural Product Library

Mass Spectrometry Human Metabolite Library

Diarrhea-Related Traditional Chinese Medicine Active Compound Library

Natural Product Diversity Scaffold Library

Lactylation Compound Library

Mass Spectrometry Natural Product Library

Publications Citing Use of MedChemExpress (MCE) Kirenol

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