Art. -Nr.: HY-183402

FLLL12

Name: FLLL12
Brand: MedChemExpress
SKU: HY-183402
Availability: PreOrder

(Synonyms: GO-Y026)

FLLL12 (GO-Y026) is a curcumin analog anticancer agent. FLLL12 inhibits the phosphorylation of AKT, Bcl-2, Bid, EGFR, mTOR, FOXO1a, FOXO3a, STAT3, HER2/neu, as well as pancreatic AKT/STAT3; upregulates the expression of Bim and DR5; and activates PTPs. FLLL12 regulates downstream pathways, induces mitochondria-mediated and DR5-dependent extrinsic apoptosis, inhibits cancer cell viability, proliferation, anchorage-independent growth and migration, and exerts a synergistic effect with Doxorubicin (HY-15142A). FLLL12 can be used in research related to head and neck squamous cell carcinoma, breast cancer, prostate cancer, pancreatic cancer, lung cancer, colon cancer and colorectal cancer.

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CAS. Nr.: 917813-60-6
Formel: C₂₁H₂₂O₇
Molecular Weight:386.40

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

FLLL12 Chemical Structure

CAS. Nr.: 917813-60-6

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Biologische Aktivität
- Beschreibung
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
Reinheit & Dokumentation
Verweise
Calculators
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Bioz

Biologische Aktivität

Beschreibung

IC₅₀ & Target

^[2]^[6]

STAT3

Bcl-2

Bim

mTOR

FOXO1a

FOXO3a

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FOXO1
FOXO3

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Cellular Effect

Cell Line	Type	Value	Description	References
HCT-116	GI₅₀	0.8 μM Compound: GO-Y026	Growth inhibition of human HCT116 cells after 48 hrs by MTS assay Growth inhibition of human HCT116 cells after 48 hrs by MTS assay	[PMID: 20060305]
HT-29	IC₅₀	2.24 μM Compound: C9	Cytotoxicity against human HT-29 cells after 72 hrs by MTT assay Cytotoxicity against human HT-29 cells after 72 hrs by MTT assay	[PMID: 22551677]
LNCaP	IC₅₀	2.5 μM Compound: 19	Antiproliferative activity against human LNCAP cells after 72 hrs by MTT assay Antiproliferative activity against human LNCAP cells after 72 hrs by MTT assay	[PMID: 19249204]
MCF7	IC₅₀	1.7 μM Compound: 19	Antiproliferative activity against human MCF7 cells after 72 hrs by MTT assay Antiproliferative activity against human MCF7 cells after 72 hrs by MTT assay	[PMID: 19249204]
MDA-MB-231	IC₅₀	2.7 μM Compound: 19	Antiproliferative activity against human MDA-MB-231 cells after 72 hrs by MTT assay Antiproliferative activity against human MDA-MB-231 cells after 72 hrs by MTT assay	[PMID: 19249204]
PANC-1	IC₅₀	2.23 μM Compound: C9	Cytotoxicity against human PANC1 cells after 72 hrs by MTT assay Cytotoxicity against human PANC1 cells after 72 hrs by MTT assay	[PMID: 22551677]
PC-3	IC₅₀	3.6 μM Compound: 19	Antiproliferative activity against human PC3 cells after 72 hrs by MTT assay Antiproliferative activity against human PC3 cells after 72 hrs by MTT assay	[PMID: 19249204]
PC-3	IC₅₀	3.41 μM Compound: C9	Cytotoxicity against human PC3 cells after 72 hrs by MTT assay Cytotoxicity against human PC3 cells after 72 hrs by MTT assay	[PMID: 22551677]

In Vitro

FLLL12 (GO-Y026) potently inhibits the growth of human colon cancer HCT-116 cells after 48 h exposure, with a GI₅₀ value of 0.8 μM^[1].
FLLL12 (0.5-5 μM; 72 h) potently inhibits the viability of MDA-MB-468, MDA-MB-231, SK-BR-3, BT-474, MDA-MB-453, MCF-7, PC-3 and DU145 cancer cells, with IC₅₀ values of 0.3, 2.7, 3.8, 1.8, 1.3, 1.7, 3.6 and 3 μM, respectively, while showing extremely low toxicity against the normal human lung fibroblast cell line WI-38^[2].
FLLL12 (1-10 μM; 24 h) significantly inhibits the DNA-binding activity of STAT3 in MDA-MB-231, SK-BR-3 and DU145 cancer cells, and suppresses STAT3-dependent transcriptional activity in stably transfected MDA-MB-231 cells in a dose-dependent manner^[2].
FLLL12 (1-5 μM; 2 weeks) inhibits anchorage-independent colony formation in MDA-MB-231 and SK-BR-3 breast cancer cells. At the concentration of 5 μM, it reduces the number of colonies in MDA-MB-231 cells by approximately 95% and almost completely suppresses colony formation in SK-BR-3 cells^[2].
FLLL12 (5-10 μM; 4 h) inhibits the migration of MDA-MB-231 breast cancer cells in a dose-dependent manner, reducing the wound healing rate to approximately 65% and 28% of that in the control group at concentrations of 5 μM and 10 μM, respectively, with no significant cytotoxicity^[2].
FLLL12 (5 μM; 72 h) acts synergistically with Doxorubicin (HY-15142A) (100-400 nM) to inhibit the viability of MDA-MB-231 breast cancer cells, with a combination index value <1^[2].
FLLL12 (1.0-20 μM; 72 h) potently inhibits the viability of human pancreatic cancer cells including PANC-1, BXPC-3, MIA-PACA-2, ASPC-1 and HPAC, with IC₅₀ values ranging from 0.91 to 3.43 μmol/l; this compound exhibits stronger activity in HPDE cells (IC₅₀ 0.26 μmol/l), while exerting minimal effects on normal human bladder cells (IC₅₀ 886.76 μmol/l)^[3].
FLLL12 (72 h) potently inhibits the growth of human lung cancer premalignant and malignant cell lines, with IC₅₀ values ranging from 0.63 to 1.87 μM^[5].
FLLL12 (72 h) potently inhibits the viability of HCT116, HT-29 and SW480 human colorectal cancer cells, with IC₅₀ values of 2.49 μM, 3.35 μM and 1.17 μM, respectively; meanwhile, this compound exhibits low toxicity to WI-38 human normal lung fibroblasts (IC₅₀ > 1000 μM)^[4].
FLLL12 (72 h) potently inhibits the growth of the premalignant cell line MSK-Leuk1 and malignant cell lines of head and neck squamous cell carcinoma (SCCHN) (Tu212, Tu177, MDA886LN, Tu686, SqCCY1, JHU022, PCI-13, UM-22B), with IC₅₀ values ranging from 0.35 to 1.55 μmol/L^[6].
FLLL12 (1-3 μM; 24-48 h) induces apoptosis in head and neck squamous cell carcinoma (SCCHN) cell lines (Tu686, MDA886LN, Tu212, UM-22B, MSK-Leuk1) in a dose- and time-dependent manner^[6].
FLLL12 (1-3 μM; 24 h) inhibits the phosphorylation of mTOR, S6, 4EBP1, FOXO1a and FOXO3a in Tu212, Tu686 and MSK-Leuk1 head and neck squamous cell carcinoma cells^[6].
FLLL12 (1-2 μM) induces mitochondria-mediated endogenous apoptosis in Tu212 head and neck squamous cell carcinoma cells by promoting the release of cytochrome C from mitochondria into the cytoplasm^[6].
FLLL12 (1-3 μM; 24 h) regulates the expression of Bcl-2 family proteins in Tu212 and Tu686 head and neck squamous cell carcinoma cells; it decreases the levels of Bcl-2 and full-length Bid, and increases the level of Bim, thereby promoting cell apoptosis^[6].
FLLL12 (2-3 μM; 48 h) induces apoptosis in Tu686 head and neck squamous cell carcinoma (SCCHN) cells, while overexpression of Bcl-2 significantly attenuates this effect, confirming that Bcl-2 is a key mediator of the pro-apoptotic effect of FLLL12^[6].
FLLL12 (1-3 μM) upregulates the expression of Bcl-2 mRNA in Tu212 and Tu686 head and neck squamous cell carcinoma cells, indicating that its inhibitory effect on Bcl-2 protein occurs at the translational level^[6].
FLLL12 (1-3 μM) inhibits the expression of EGFR and AKT mRNA in Tu212 and Tu686 head and neck squamous cell carcinoma (SCCHN) cells, indicating that its inhibitory effect on EGFR and AKT proteins occurs at the transcriptional level^[6].
FLLL12 (3 μM; 48 h) induces apoptosis in Tu686 head and neck squamous cell carcinoma (SCCHN) cells, and knockdown of Bim significantly attenuates this effect, confirming that Bim is a key mediator of the pro-apoptotic action of FLLL12^[6].
FLLL12 (3 μM; 48 h) induces apoptosis in Tu686 head and neck squamous cell carcinoma (SCCHN) cells, and knockdown of Bid significantly attenuates this effect, confirming that Bid is a key mediator of the apoptotic effect of FLLL12^[6].
FLLL12 (5-10 μM; 24 h) downregulates the expression of HER2/neu in BT-474, SK-BR-3 and MDA-MB-453 breast cancer cells, and inhibits the phosphorylation of AKT Ser473 in MDA-MB-453 breast cancer cells and PC-3 prostate cancer cells. Meanwhile, FLLL12 increases the levels of cleaved PARP in BT-474, SK-BR-3, MDA-MB-453 and PC-3 cells, and elevates the levels of cleaved caspase-3 in SK-BR-3, MDA-MB-453 and PC-3 cells, indicating that it induces cell apoptosis^[2].
FLLL12 (10 μM; 24 h) inhibits the phosphorylation of STAT3 (Tyr705) in MDA-MB-231, SK-BR-3 and DU145 cancer cells, induces apoptosis in these cancer cells, and does not trigger apoptosis in normal HMEC or WI-38 cells^[2].
FLLL12 (5-10 μM; 24-48 h) inhibits the phosphorylation of STAT3 and induces apoptosis in PANC-1, BXPC-3 and HPAC human pancreatic cancer cells via cleaved caspase-3 or cleaved PARP. After 24-48 h of treatment, 10 μmol/l of this agent also inhibits the phosphorylation of AKT in BXPC-3 cells^[3].
FLLL12 (5-10 μM; 24-48 h) inhibits STAT3 phosphorylation and induces apoptosis in PANC-1, HPAC and MIA-PACA-2 human pancreatic cancer cells^[3].
FLLL12 (3-5 μM; 48 h) induces approximately 80% apoptosis in premalignant and malignant human lung cancer cell lines in a dose- and time-dependent manner^[5].
FLLL12 induces apoptosis in human lung cancer cell lines H1299, H292 and A549, which is evidenced by the cleavage of caspase-3 and PARP^[5].
FLLL12 (24 h) induces apoptosis in human lung cancer cell lines A549, H1299 and H292 via a pathway dependent on death receptor 5 (DR5) and requiring the involvement of caspase-8 and Bid, in which DR5 and caspase-8 play more critical roles than Bid^[5].
FLLL12 (incubated for 24 h) activates caspase-8 and cleaves Bid into tBid in human lung cancer cell lines A549 and H1299, thereby inducing apoptosis^[5].
FLLL12 (24 h) induces the expression of DR5 and subsequent apoptosis in the human lung cancer cell line A549, and this process depends on the activation of protein tyrosine phosphatases (PTPs); because inhibition of PTPs (but not alkaline phosphatase) blocks these effects^[5].
FLLL12 induces apoptosis in human lung cancer cell lines H₂92 and H₁299 in a p53- and p73-independent manner^[5].
FLLL12 (2.5-5 μM; 24 h) induces apoptosis in human colorectal cancer cells HCT116, HT-29 and SW480 (as confirmed by cleaved PARP and cleaved caspase-3), but fails to induce the production of cleaved PARP in normal human lung fibroblasts WI-38 and mammary epithelial cells MCF-10A^[4].
FLLL12 (1-3 μM; 24-48 h) inhibits the phosphorylation and total protein levels of EGFR and AKT in Tu212, Tu686 and MSK-Leuk1 head and neck squamous cell carcinoma (SCCHN) cells, with the inhibition of phosphorylated AKT occurring earlier than the downregulation of total AKT^[6].
FLLL12 (1-3 μM; 48 h) induces apoptosis in Tu686 SCCHN cells, and overexpression of constitutively active AKT significantly attenuates this effect, confirming that AKT inhibition is a key mediator of the pro-apoptotic effect of FLLL12^[6].
Treatment of immortalized human pancreatic ductal epithelial (HPDE) cells with FLLL12 (5 μM; 24-48 h) for 24-48 h does not induce apoptosis (detected via activated caspase-3)^[3].
FLLL12 (24 h; 2 h) post-transcriptionally (possibly at the translational level) regulates the expression of DR5 in human lung cancer cell lines A549 and H1299, with no effect on DR5 mRNA levels^[5].

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

Apoptosis Analysis^[6]

Cell Line:

Tu686, MDA886LN, Tu212, UM-22B, MSK-Leuk1
Concentration:

1-3 μM (24 h incubation); 1-3 μM (48 h incubation); 1-3 μM (24 h incubation in MSK-Leuk1 cells)
Incubation Time:

24 h; 48 h
Result:

Induced apoptosis in a dose- and time-dependent manner across all tested cell lines.
Induced approximately 80% apoptosis in most cell lines after treatment with 1 to 3 μmol/L for 48 hours.
Induced over 80% apoptosis in MSK-Leuk1 cells after 24 hours of treatment with 3 μmol/L.

Western Blot Analysis^[6]

Cell Line:

Tu212, Tu686, MSK-Leuk1
Concentration:

1-1.5 μM (Tu212); 2-3 μM (Tu686); 1-3 μM (MSK-Leuk1)
Incubation Time:

24 h
Result:

Markedly induced cleavage of PARP (a marker of apoptosis) in all three tested cell lines.
Strongly inhibited phosphorylation of mTOR, S6, and 4EBP1 (components of the mTOR-mediated protein translational pathway).
Inhibited phosphorylation of FOXO1a and FOXO3a at multiple sites in all three tested cell lines.

Western Blot Analysis^[6]

Cell Line:

Tu212, Tu686
Concentration:

1-1.5 μM (Tu212); 2-3 μM (Tu686)
Incubation Time:

24 h
Result:

Decreased protein expression of antiapoptotic Bcl-2 and full-length proapoptotic Bid.
Increased protein expression of proapoptotic Bim.
Left expression of Bcl-xL and Mcl-1 mostly unchanged.

Apoptosis Analysis^[6]

Cell Line:

Tu686
Concentration:

2, 3 μM
Incubation Time:

48 h
Result:

Overexpression of Bcl-2 significantly protected Tu686 cells from FLLL12-induced apoptosis, with apoptosis rates reduced by approximately 50% compared to control cells at both tested concentrations.

Apoptosis Analysis^[6]

Cell Line:

Tu686
Concentration:

3 μM
Incubation Time:

48 h
Result:

Ablation of Bim expression significantly protected Tu686 cells from FLLL12-induced apoptosis, reducing apoptosis rates from approximately 45% in control siRNA-transfected cells to approximately 20% in Bim siRNA-transfected cells.\n
Ablation of Bid expression significantly protected Tu686 cells from FLLL12-induced apoptosis, reducing apoptosis rates from approximately 55% in control siRNA-transfected cells to approximately 30% in Bid siRNA-transfected cells.

Western Blot Analysis^[6]

Cell Line:

Tu212, Tu686, MSK-Leuk1
Concentration:

1-1.5 μM (Tu212); 2, 3 μM (Tu686); 1-3 μM (MSK-Leuk1)
Incubation Time:

24 h; 48 h
Result:

Potently inhibited phosphorylation of EGFR and AKT, and also reduced total EGFR and AKT protein levels in all three tested cell lines, with greater potency than curcumin.
Inhibition of phosphorylated AKT preceded inhibition of total AKT at 12 hours of treatment.

Apoptosis Analysis^[6]

Cell Line:

Tu686
Concentration:

1-3 μM
Incubation Time:

48 h
Result:

Overexpression of CA-AKT significantly protected Tu686 cells from FLLL12-induced apoptosis, reducing apoptosis rates by approximately 40% to 50% compared to control cells at tested concentrations.
Overexpression of CA-AKT inhibited FLLL12-induced PARP cleavage, caspase-3 activation, and Bim upregulation, and reduced FLLL12-mediated inhibition of Bcl-2.

Western Blot Analysis^[2]

Cell Line:

BT-474, SK-BR-3, MDA-MB-453, PC-3
Concentration:

5-10 μM
Incubation Time:

24 h
Result:

Downregulated HER2/neu protein expression in BT-474, SK-BR-3, and MDA-MB-453 breast cancer cells.
Inhibited AKT phosphorylation (Ser473) in MDA-MB-453 breast cancer cells and PC-3 prostate cancer cells, and decreased total AKT expression in MDA-MB-453 cells.
Induced apoptosis in all tested cancer cell lines, as evidenced by increased levels of cleaved PARP and cleaved caspase-3.

Western Blot Analysis^[2]

Cell Line:

MDA-MB-231, SK-BR-3, DU145, HMEC, WI-38
Concentration:

10 μM
Incubation Time:

24 h
Result:

Inhibited STAT3 phosphorylation (Tyr705) in MDA-MB-231, SK-BR-3, and DU145 cancer cells, without affecting ERK1/2 phosphorylation.
Induced apoptosis in these cancer cells, as shown by increased cleaved PARP and cleaved caspase-3 levels.
Did not induce cleaved PARP or cleaved caspase-3 in normal HMEC or WI-38 cells.

Cell Migration Assay ^[2]

Cell Line:

MDA-MB-231
Concentration:

5-10 μM
Incubation Time:

4 h
Result:

Impaired MDA-MB-231 cell migration.
At 5 μM, reduced wound healing to ~65% of control levels; at 10 μM, further reduced to ~28% of control levels.
Inhibitory effect was not due to cytotoxicity, as cell viability remained high after treatment.

Cell Viability Assay^[2]

Cell Line:

MDA-MB-231
Concentration:

5000 nM (FLLL12); 100-400 nM (doxorubicin)
Incubation Time:

72 h
Result:

All tested combinations of doxorubicin and FLLL12 resulted in CI values <1, indicating synergistic growth inhibition of MDA-MB-231 cells.

Western Blot Analysis^[3]

Cell Line:

human pancreatic cancer cell lines (PANC-1, BXPC-3, HPAC)
Concentration:

5 μM, 10 μmol/l
Incubation Time:

24-48 h
Result:

Inhibited STAT3 phosphorylation (Tyr705) and increased levels of cleaved caspase-3 in PANC-1 cells.
Inhibited STAT3 phosphorylation, induced significant levels of cleaved PARP in BXPC-3 cells; 10 μmol/l inhibited AKT phosphorylation (Ser473) in BXPC-3 cells.
Inhibited STAT3 phosphorylation and increased levels of cleaved caspase-3 in HPAC cells.

Western Blot Analysis^[3]

Cell Line:

immortalized human pancreatic duct epithelial (HPDE) cells
Concentration:

5 μM
Incubation Time:

24-48 h
Result:

Did not induce increased levels of cleaved caspase-3.

Western Blot Analysis^[3]

Cell Line:

human pancreatic cancer cell lines (PANC-1, HPAC, MIA-PACA-2)
Concentration:

5 μM, 10 μM
Incubation Time:

24-48 h
Result:

Inhibited STAT3 phosphorylation and induced cleaved caspase-3 at levels similar to the curcumin analogue GO-Y030 in PANC-1 cells.
Inhibited STAT3 phosphorylation and induced cleaved caspase-3 in HPAC cells.
Induced cleaved PARP and cleaved caspase-3 at levels similar to GO-Y030 in MIA-PACA-2 cells.

Apoptosis Analysis^[5]

Cell Line:

premalignant and malignant human lung cancer cell lines
Concentration:

3-5 μM
Incubation Time:

48 h
Result:

Induced apoptosis in a dose- and time-dependent manner.
Induced ~80% apoptosis in lung cancer cell lines, a level of apoptosis that required 15-30 μM curcumin to achieve.

Western Blot Analysis^[4]

Cell Line:

HCT116, HT-29, SW480 human colorectal cancer cells, WI-38 normal human lung fibroblasts, MCF-10A immortalized human mammary epithelial cells
Concentration:

2.5 μM, 5 μM
Incubation Time:

24 h
Result:

Induced increased levels of cleaved PARP and cleaved caspase-3 in HCT116 cells at 2.5 μM and 5 μM.
Induced increased levels of cleaved PARP and slightly increased levels of cleaved caspase-3 in HT-29 cells at 5 μM.
Induced increased levels of cleaved PARP and cleaved caspase-3 in SW480 cells at 5 μM.
Did not induce cleaved PARP in WI-38 cells or MCF-10A cells.

Parmacokinetics

Species	Dose	Route	T_max	C_max	T_1/2	AUC_last	Clearance (CL)
Mice^[6]	200 mg/kg	p.o.	0.5 h	241.5 ng/mL	4.8 h	418.1 ng·h/mL	449.2 L/h/kg

In Vivo

FLLL12 (50 mg/kg; i.p.; once daily, 5 days per week; for 17 days) significantly inhibits the growth of head and neck squamous cell carcinoma xenografts in nude mice, with no systemic toxicity observed^[6].

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

Animal Model:

athymic nu/nu (female, 4 to 6 weeks old, ~20 g, subcutaneous xenograft of 4×10⁶ Tu686 cells)^[6]
Dosage:

50 mg/kg
Administration:

i.p.; once daily, 5 days per week; 17 days
Result:

Reduced average tumor volume to ~600 mm³ at day 17, compared with ~1200 mm³ in vehicle and curcumin-treated groups (P < 0.05).
Showed no significant changes in body weight.
Exhibited no notable toxicities in histopathological analysis of major organs.

Chemical Information

CAS. Nr. 917813-60-6
Molecular Weight 386.40
Formel C₂₁H₂₂O₇
SMILES

COC(C=C1/C=C/C(/C=C/C2=CC(OC)=C(C(OC)=C2)O)=O)=C(C(OC)=C1)O
Synonyms

GO-Y026
Versand

Room temperature in continental US; may vary elsewhere.
Speicherung

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

Reinheit & Dokumentation

Handling Instructions (2659 KB)

Verweise

[1]. Yamakoshi H, et al. Structure-activity relationship of C5-curcuminoids and synthesis of their molecular probes thereof. Bioorganic & medicinal chemistry. 2010 Feb;18(3):1083-92. [Content Brief]

[2]. Lin L, et al. New curcumin analogues exhibit enhanced growth-suppressive activity and inhibit AKT and signal transducer and activator of transcription 3 phosphorylation in breast and prostate cancer cells. Cancer Sci. 2009;100(9):1719-1727.

[3]. Friedman L, et al. Curcumin analogues exhibit enhanced growth suppressive activity in human pancreatic cancer cells. Anti-cancer drugs. 2009 Jul;20(6):444-9. [Content Brief]

[4]. Cen L, et al. New structural analogues of curcumin exhibit potent growth suppressive activity in human colorectal carcinoma cells. BMC cancer. 2009 Mar 30;9:99. [Content Brief]

[5]. Haque A er al. FLLL12 induces apoptosis in lung cancer cells through a p53/p73-independent but death receptor 5-dependent pathway. Cancer Lett. 2015 Jul 28;363(2):166-75.

[6]. Anisuzzaman AS, et al. Preclinical In Vitro, In Vivo, and Pharmacokinetic Evaluations of FLLL12 for the Prevention and Treatment of Head and Neck Cancers. Cancer prevention research (Philadelphia, Pa.). 2016 Jan;9(1):63-73. [Content Brief]

Calculators

Molaritätsrechner

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

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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)}

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FLLL12

Alle Akt Isoform-spezifische Produkte anzeigen

Alle Bcl-2 Family Isoform-spezifische Produkte anzeigen

Alle EGFR Isoform-spezifische Produkte anzeigen

Alle mTOR Isoform-spezifische Produkte anzeigen

Alle FOXO Isoform-spezifische Produkte anzeigen

Alle STAT Isoform-spezifische Produkte anzeigen