2. Autophagy
  3. Autophagy
  4. PHY34

PHY34 is an inhibitor that inhibits ATP6V0A2 and CAS thereby inhibiting autophagy, and has a nanomolar effect. PHY34 inhibits cancer cell growth by inducing apoptosis and inhibits tumor growth in xenograft models. PHY34 can be used for research on high grade serous ovarian cancer.

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

PHY34 Chemical Structure

PHY34 Chemical Structure

CAS No. : 2130033-55-3

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PHY34 Related Antibodies

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Description

PHY34 is an inhibitor that inhibits ATP6V0A2 and CAS thereby inhibiting autophagy, and has a nanomolar effect. PHY34 inhibits cancer cell growth by inducing apoptosis and inhibits tumor growth in xenograft models. PHY34 can be used for research on high grade serous ovarian cancer[1][2].

IC50 & Target

ATP6V0A2, cellular apoptosis susceptibility (CAS)[2]
In Vitro

PHY34 (0.001 nM-50 μM, 72 h) inhibits various cancer cells growth with nanomolar potency through activation of apoptosis based on enhanced cPARP levels and has the highest potency in HGSOC cell lines[1].
PHY34 (100 nM, 1 μM; 24 h) blocks the final breakdown of the autolysosomes in OVCAR8 at 100 nM, and in OVCAR3 at 1 μM, respectively[1].
PHY34 (10 nM, 24 h) inhibits the late-stage autophagy that precedes apoptosis induction in OVCAR8[1].
PHY34 (100 nM, 48 h) inhibits the late-stage autophagy that precedes apoptosis induction in OVCAR3[1].
PHY34 (0.01 nM-2 μM, 72 h) induces cell death in the presence of wild-type V0A2, but not V823I mutants in H4 cell[2].
PHY34 (10, 100 nM; 48 h, 72 h) changes subcellular localization of nuclear multiple proteins[2].
PHY34 (20 μM, 1 h) binds specificity with ATP6V0A2 subunit[2].

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

PHY34 Related Antibodies

Cell Viability Assay[1][2]

Cell Line: OVCAR8, OVCAR3, HT-29, MDA-MB-435, MDA-MB-231, IOSE80, FT33
Concentration: 0.001 nM-50 μM
Incubation Time: 72 h
Result: Inhibited the growth of various cancer cells with IC50 values of 4 nM(OVCAR8, OVCAR3), 43.3 nM(HT-29) , 23 nM(MDA-MB-435) , 5.2 nM(MDA-MB-231).
Exhibited no toxicity to IOSE80 and FT33 (IC50 >50 μM).

Cell Viability Assay[2]

Cell Line: H4
Concentration: 0.01 nM-2 μM
Incubation Time: 72 h
Result: Inhibited mutant cell with an IC50 value of 246 pM that was 1000-fold more potent than HTP-013(434 nM).
Conferred resistance in V8231 mutation and no impact activity in T216A mutation.

Apoptosis Analysis[1]

Cell Line: OVCAR8, OVCAR3
Concentration: 10 nM, 100 nM
Incubation Time: 72 h
Result: Increased the number of cells in early and late apoptosis in OVCAR8 and OVCAR3 at 10 nM and 100 nM, respectively.

Cell Autophagy Assay[1]

Cell Line: Hela
Concentration: 9.31 fM-20 μM
Incubation Time: 4 h
Result: Sustained high levels of LC3B puncta with an EC50 value of 2 nM.
Inhibited autophagy with an EC50 value of 3.9 nM.

Cell Autophagy Assay[2]

Cell Line: OVCAR3
Concentration: 5 nM
Incubation Time: 4 h
Result: Inhibited autophagy with an ED50 value of 6.29 nM, and was more potent than bafilomycin A1 (HY-100558) with an ED50 value of 29.1 nM.

Western Blot Analysis[1][2]

Cell Line: OVCAR8, OVCAR3, OVCAR4
Concentration: 10 nM, 100 nM
Incubation Time: 48 h, 72 h
Result: Increased cPARP levels in OVCAR8 after 48 h at 10 nM, in OVCAR4 and OVCAR3 after 72 h at 100 nM, respectively.
Reversed the conversion of PARP to cPARP combined with RAP (HY-10219) of 1 μM.

Western Blot Analysis[2]

Cell Line: OVCAR8, OVCAR3, OVCAR4
Concentration: 10 nM
Incubation Time: 24 h, 48 h, 72 h
Result: Promoted histone H3, LAMP1/2, ACSS2, and PCNA nuclear protein accumulation at 48 h.
Reduced expression of KPNA2 (Karyopherin subunit alpha 2) with time-dependent manner.
Increased nuclear accumulation of mutant p53 at 48 h.
In Vivo

PHY34 (0.75 mg/kg, i.p., 3 times a week for 3 weeks) inhibits tumor growth and reduces Ki67 expression in tumor tissue in a female nude mouse tumor bearing model constructed by OVCAR8[1].

PHY34 Pharmacokinetics[1]

药代动力学分析[1]

Parameter Units IV IP PO
Dose mg/kg 0.6 1.8 75
Dose nmol 1029.9 3089.8 128742.1
T1/2 hr 6.2 8.4 12.3
Tmax hr 0.08 0.25 0.25
Cmax nmol/L 288.8 519.5 323.6
AUClast hr*nmol/L 198.8 360.5 599.9
AUCinf hr*nmol/L 215.8 366.5 663.3
Vz L/kg 42.7 101.6 3430.3
CI L/hr/kg 4.8 8.4 194.1
MRT hr 6.1 1.9 7.8
F* % - 56.6 2.5

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

Animal Model: OVCAR8-induced xenograft models in female nude mice[1].
Dosage: 0.75 mg/kg, three times a week for three weeks
Administration: Intraperitoneal injection (i.p.)
Result: Decreased tumor burden based on average abdominal radiant efficiency with no gross toxicity through analysis of fluorescence imaging.
Molecular Weight

582.55

Formula

C30H30O12
CAS No.
SMILES

O=C1C2=C(C3=CC=C(OCO4)C4=C3)C5=CC(OC)=C(OC)C=C5C(O[C@H]6[C@@H]([C@]7([H])[C@](OC(C)(O7)C)([H])[C@H](O6)CO)O)=C2CO1
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References
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PHY34 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

PHY342130033-55-3PHY 34PHY-34AutophagyOVCAR8OVCAR3HT-29MDA-MB-435MDA-MB-231IOSE80Helaxenograft model high grade serous ovarian cancerInhibitorinhibitorinhibit

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