Cat. No.: HY-116032

PAO-PDT

PAO-PDT is an organoarsenic inhibitor of thioredoxin reductase (TrxR), with an IC₅₀ of 33 nM. PAO-PDT can bind to the C-terminal selenocysteine/cysteine pair of TrxR and convert the enzyme into an NADPH oxidase, which increases reactive oxygen species levels and impairs mitochondrial respiratory function, thereby inducing apoptosis in leukemia cells. PAO-PDT can be used for leukemia research.

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

CAS No.: 256348-71-7
Formula: C₉H₁₂AsNS₂
Molecular Weight:273.24

Storage:

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

PAO-PDT Chemical Structure

CAS No.: 256348-71-7

Price

Stock

Quantity

Amount: USD 0.00

* Please select Quantity before adding items.

Use of MCE Products

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
Chemical Information
Purity & Documentation
References
Calculators
Help & FAQs
Classifications
Bioz

Biological Activity

Description

IC₅₀ & Target

^[2]

TrxR

33 nM (IC₅₀)

All TrxR Isoforms :

TrxR1
TrxR2

Cellular Effect

Cell Line	Type	Value	Description	References
HL-60	IC50	0.7 μM	Cytotoxicity against human promyelocytic leukemia HL-60 cells assessed as inhibition of proliferation incubated for 48 hrs by MTT assay. Cytotoxicity against human promyelocytic leukemia HL-60 cells assessed as inhibition of proliferation incubated for 48 hrs by MTT assay.	41338133
HL-60	IC50	0.6 μM	Cytotoxicity against human promyelocytic leukemia HL-60 cells assessed as inhibition of proliferation incubated for 72 hrs by MTT assay. Cytotoxicity against human promyelocytic leukemia HL-60 cells assessed as inhibition of proliferation incubated for 72 hrs by MTT assay.	41338133
SMMC-7721	IC50	2.8 μM	Cytotoxicity against human hepatocellular carcinoma 7721 cells assessed as inhibition of proliferation incubated for 48 hrs by MTT assay. Cytotoxicity against human hepatocellular carcinoma 7721 cells assessed as inhibition of proliferation incubated for 48 hrs by MTT assay.	41338133
HeLa	IC50	3.4 μM	Cytotoxicity against human cervical cancer HeLa cells assessed as inhibition of proliferation incubated for 48 hrs by MTT assay. Cytotoxicity against human cervical cancer HeLa cells assessed as inhibition of proliferation incubated for 48 hrs by MTT assay.	41338133
HepG2	IC50	> 10 μM	Cytotoxicity against human hepatocellular carcinoma HepG2 cells assessed as inhibition of proliferation incubated for 48 hrs by MTT assay. Cytotoxicity against human hepatocellular carcinoma HepG2 cells assessed as inhibition of proliferation incubated for 48 hrs by MTT assay.	41338133
L02	IC50	10.2 μM	Cytotoxicity against human normal liver L02 cells assessed as inhibition of proliferation by MTT assay. Cytotoxicity against human normal liver L02 cells assessed as inhibition of proliferation by MTT assay.	41338133
HEK-293T	IC50	2.7 μM	Cytotoxicity against human embryonic kidney HEK 293T cells assessed as inhibition of proliferation by MTT assay. Cytotoxicity against human embryonic kidney HEK 293T cells assessed as inhibition of proliferation by MTT assay.	41338133
HL-60	IC50	1.4 μM	Inhibition of cellular thioredoxin reductase activity in human promyelocytic leukemia HL-60 cells. Inhibition of cellular thioredoxin reductase activity in human promyelocytic leukemia HL-60 cells.	41338133
HL-60	IC50	0.81 μM	Cytotoxicity against human HL-60 malignant cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay. Cytotoxicity against human HL-60 malignant cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay.	30665675
HeLa	IC50	4.86 μM	Cytotoxicity against human HeLa malignant cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay. Cytotoxicity against human HeLa malignant cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay.	30665675
SMMC-7721	IC50	5.24 μM	Cytotoxicity against human SMMC-7721 malignant cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay. Cytotoxicity against human SMMC-7721 malignant cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay.	30665675
HepG2	IC50	2.27 μM	Cytotoxicity against human HepG2 malignant cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay. Cytotoxicity against human HepG2 malignant cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay.	30665675

In Vitro

PAO-PDT (compound 4) selectively and potently inhibits the proliferation of human promyelocytic leukemia HL-60 cells within 48-72 h, with IC₅₀ values of 0.7 μM (48 h) and 0.6 μM (72 h), respectively, while exhibiting low cytotoxicity against other cancer cell lines and normal cells^[1].
PAO-PDT (2.0-5.0 μM; 48 h) exhibits weak effects on human embryonic kidney HEK-TrxR1 cells with overexpressed TrxR, whereas human cervical carcinoma HeLa-shTrxR1 cells with TrxR knockdown are more sensitive to PAO-PDT, which confirms that TrxR targeting mediates the cytotoxicity of PAO-PDT^[1].
PAO-PDT (48 h) inhibits the proliferation of HL-60 cells, with an IC₅₀ of 0.70 μM after 48 h of incubation^[2].
PAO-PDT (compound 8) (48 h) potently inhibits the viability of HL-60 leukemia cells with an IC₅₀ of 0.81 μM, and exhibits low cytotoxicity against HeLa, SMMC-7721, and HepG2 cells^[4].
PAO-PDT (24-48 h) inhibits the viability of NB4, HL-60, HeLa, SGC7901, MCF-7, and HEK293 cells in vitro, with the highest potency against NB4 cells (IC₅₀ = 0.82 μM at 48 h)^[3].
PAO-PDT (0.6-3.6 μM; 1-8 h) induces a time- and concentration-dependent decrease in the viability of NB4 cells in vitro, and after incubation with 3.6 μM PAO-PDT for 8 h, the cell viability decreases to approximately 0.38^[3].
PAO-PDT (50-200 nM) potently inhibits the purified wild-type TrxR at concentrations of 50 nM and above, but does not inhibit the purified U498C mutant TrxR at the same concentrations^[1].
PAO-PDT inhibits recombinant rat wild-type thioredoxin reductase with an IC₅₀ of approximately 33 nM, and exhibits no significant inhibitory effect on U498C TrxR, GR, GPx, or Trx^[1].
PAO-PDT (1-2 μM; 12-24 h) inhibits the activity of cellular thioredoxin reductase in human promyelocytic leukemia HL-60 cells, with an IC₅₀ of approximately 1.4 μM; it also directly binds to endogenous TrxR1 and upregulates the expression of TrxR1 protein at concentrations of 1 μM (24 h) and 2 μM (12 h)^[1].
PAO-PDT (1-10 μM; 12-24 h) induces concentration-dependent cellular thiol depletion in human promyelocytic leukemia HL-60 cells, and the degree of depletion after 24 h is greater than that after 12 h^[1].
PAO-PDT potently inhibits purified TrxR with an IC₅₀ of 33 nM^[2].
PAO-PDT (30 min) inhibits the activity of purified recombinant rat TrxR1 and exhibits extremely low inhibitory activity against GR^[4].
PAO-PDT (2 μM; 24 h) inhibits cellular TrxR activity in HL-60 cells by approximately 40%^[4].
PAO-PDT (1 μM; 1-2 h) induces time-dependent reactive oxygen species accumulation in human promyelocytic leukemia HL-60 cells^[1].
PAO-PDT (1.2 μM; 1-6 h) induces mild short-term ROS accumulation in NB4 cells in vitro^[3].
PDT-PAO (15-100 μM) regulates mitochondrial respiration in isolated rat liver mitochondria^[3].
PDT-PAO (0.3-2.4 μM; 24 h) increases the intracellular ROS level in NB4 cells in a concentration-dependent manner in vitro, and the induction effect reaches its peak at 2.4 μM^[3].
The cytotoxicity of PAO-PDT (0.01-2.0 μM; 48 h) against human promyelocytic leukemia HL-60 cells is inhibited by Acetylcysteine (HY-B0215) in a dose-dependent manner, while pretreatment with L-Buthionine-(S,R)-sulfoximine (HY-106376A) enhances the cytotoxicity of PAO-PDT^[1].
PAO-PDT (0.5-5 μM; 12-24 h) induces dose- and time-dependent apoptotic cell death in human promyelocytic leukemia HL-60 cells, and the proportion of apoptotic cells observed at 24 h is higher than that at 12 h^[1].
PAO-PDT (0.5-2 μM; 24 h) induces concentration-dependent activation of caspase-3 in human promyelocytic leukemia HL-60 cells after 24 h of treatment^[1].
PAO-PDT (0.5-5 μM; 24 h) induces apoptotic nuclear morphology in human promyelocytic leukemia HL-60 cells after 24 h of treatment, characterized by nuclear pyknosis and high fluorescence intensity^[1].
PDT-PAO (0.6-2.4 μM; 4-24 h) reduces the total thiol level in NB4 cells in a concentration- and time-dependent manner, with the most potent reduction observed after treatment with 2.4 μM for 24 h^[3].
PDT-PAO (1.2-2.4 μM; 24 h) increases the level of cytochrome c in NB4 cells^[3].
PAO-PDT (1.2 μM; 1-6 h) induces a slight time-dependent collapse of mitochondrial membrane potential in NB4 cells in vitro^[3].
PAO-PDT (1.2-2.4 μM; 24 h) reduces the intracellular ATP level in NB4 cells in a concentration-dependent manner in vitro. After incubation with 2.4 μM PAO-PDT for 24 h, the ATP level decreases to ~5 μmol/g protein^[3].
PAO-PDT (50-200 μM) inhibits thermogenesis in isolated mitochondria from NB4 cells in vitro. At 100 μM, it reduces the maximum power output to 96.9 μW and slows the rate constants of the activity recovery phase, steady-state rise phase, and decline phase^[3].
PDT-PAO (1-5 μM; 2.5-5 h) inhibits PDHC activity in NB4 cells, and the enzyme activity in the treatment groups at concentrations of 1 μM and 5 μM (incubated for 2.5 h) as well as 2.4 μM (incubated for 5 h) decreases compared with the untreated control group^[3].
PDT-PAO (2.4 μM; 24 h) reduces the viability of NB4 cells, and this effect is reversed in a concentration-dependent manner upon combined treatment with LA^[3].
PDT-PAO (1.5-2 μM; 24 h) reduces the viability of NB4 cells, and this effect is observed at both concentrations of 1.5 μM and 2 μM (with 24 h incubation); however, this effect is reversed in a concentration-dependent manner upon combined treatment with DL-Dithiothreitol (DTT) (HY-15917), Dimethyl phthalate (DMP) (HY-N7106), or Succimer (DMSA) (HY-B1768)^[3].
PDT-PAO (0.6-3.6 μM; 12-24 h) reduces the viability of NB4 cells in a concentration- and time-dependent manner, with incubation durations of 12 h or 24 h; pretreatment with 50 μM DL-Buthionine-(S,R)-sulfoximine (BSO) (HY-106376) enhances this cytotoxic effect^[3].
The combination of PDT-PAO (25-150 μM) with 4 μM Ca²⁺ induces swelling of isolated rat liver mitochondria in a concentration-dependent manner^[3].
PDT-PAO (50-200 μM) induces negligible H⁺ permeability of the mitochondrial inner membrane in isolated rat liver mitochondria, and only causes slight alterations in K⁺ permeability ^[3].
Incubation with PDT-PAO (100 μM; 30 min) for 30 min induces ultrastructural damage in isolated rat liver mitochondria^[3].

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

Cell Cytotoxicity Assay^[1]

Cell Line:

human promyelocytic leukemia HL-60 cells, human hepatocellular carcinoma 7721 cells, human cervical cancer HeLa cells, human hepatocellular carcinoma HepG2 cells, human normal liver L02 cells, human embryonic kidney HEK 293T cells
Concentration:

0.7 μM (HL-60 cells, 48 h); 0.6 μM (HL-60 cells, 72 h); 2.8 μM (7721 cells, 48 h); 3.4 μM (HeLa cells, 48 h); 10.2 μM (L02 cells); 2.7 μM (HEK 293T cells)
Incubation Time:

48 h (HL-60, 7721, HeLa cells); 72 h (HL-60 cells); null (L02, HEK 293T cells)
Result:

Exhibited selective, potent cytotoxicity toward HL-60 cells, with IC₅₀ values of 0.7 μM (48 h) and 0.6 μM (72 h).
Showed lower cytotoxicity toward 7721 cells (IC₅₀ = 2.8 μM, 48 h) and HeLa cells (IC₅₀ = 3.4 μM, 48 h), with no cytotoxicity toward HepG2 cells (IC₅₀ > 10 μM, 48 h).
Displayed reduced toxicity toward normal cells, with IC₅₀ values of 10.2 μM (L02) and 2.7 μM (HEK 293T).

Cell Cytotoxicity Assay^[1]

Cell Line:

human promyelocytic leukemia HL-60 cells
Concentration:

0, 0.5, 1.0, 2.0 μM (with 0, 0.1, 1.0, 2.0 mM NAC); 0, 0.01, 0.1, 1 μM (with 100 μM BSO pre-treatment)
Incubation Time:

48 h (NAC co-treatment); 24 h (BSO pre-treatment) followed by 48 h incubation
Result:

NAC dose-dependently protected HL-60 cells from PAO-PDT-induced cytotoxicity.
BSO pre-treatment enhanced PAO-PDT cytotoxicity in HL-60 cells.

Cell Cytotoxicity Assay^[1]

Cell Line:

human embryonic kidney HEK-IRES (vector control) cells, human embryonic kidney HEK-TrxR1 (TrxR-overexpressing) cells, human cervical cancer HeLa-shNT (nontargeting shRNA control) cells, human cervical cancer HeLa-shTrxR1 (TrxR-knockdown) cells
Concentration:

2.0, 5.0 μM
Incubation Time:

48 h
Result:

HEK-TrxR1 cells (overexpressing TrxR) showed significantly higher viability than HEK-IRES control cells after PAO-PDT treatment.
HeLa-shTrxR1 cells (TrxR-knockdown) showed lower viability than HeLa-shNT control cells after PAO-PDT treatment.

Apoptosis Analysis^[1]

Cell Line:

human promyelocytic leukemia HL-60 cells
Concentration:

0, 0.5, 2, 5 μM (12 h incubation); 0, 0.5, 2, 5 μM (24 h incubation)
Incubation Time:

12 h; 24 h
Result:

Induced dose- and time-dependent apoptotic cell death in HL-60 cells, with increased apoptotic populations (early and late apoptosis) after 24 h compared to 12 h.
Maintained necrotic cell population as low as that of the control.

Apoptosis Analysis^[1]

Cell Line:

human promyelocytic leukemia HL-60 cells
Concentration:

0, 0.5, 2, 5 μM
Incubation Time:

24 h
Result:

Revealed characteristic condensed, highly fluorescent nuclei in PAO-PDT-treated HL-60 cells, confirming apoptotic morphology.

Cell Viability Assay^[4]

Cell Line:

NB4
Concentration:

0.6-3.6 μM
Incubation Time:

1 h, 4 h, 8 h
Result:

Induced time- and concentration-dependent decreases in cell viability.
Reduced viability to ~0.38 at 3.6 μM after 8 h of incubation.

Cell Viability Assay^[4]

Cell Line:

NB4
Concentration:

0.4-1.6 μM
Incubation Time:

12 h, 24 h
Result:

Had its induced cell viability loss enhanced by pre-incubation with 50 μM BSO (a GSH scavenger).

Cell Viability Assay^[3]

Cell Line:

NB4 cells
Concentration:

2.4 μM; 2.4 μM with 0.05 mM LA; 2.4 μM with 0.075 mM LA
Incubation Time:

24 h
Result:

Reduced NB4 cell viability to near 0 at 2.4 μM alone after 24 h incubation.
Increased viability to approximately 0.4 when co-incubated with 0.05 mM LA.
Increased viability to approximately 0.9 when co-incubated with 0.075 mM LA.

Cell Viability Assay^[3]

Cell Line:

NB4 cells
Concentration:

1.5 μM; 2 μM; 1.5 μM with 250 μM DTT; 1.5 μM with 500 μM DTT; 2 μM with 100 μM DMP; 2 μM with 300 μM DMP; 1.5 μM with 100 μM DMSA; 1.5 μM with 150 μM DMSA
Incubation Time:

24 h
Result:

Reduced NB4 cell viability to approximately 0.5 at 1.5 μM alone after 24 h incubation.
Increased viability to approximately 0.7 when co-incubated with 250 μM DTT.
Increased viability to approximately 0.8 when co-incubated with 500 μM DTT.
Reduced viability to approximately 0.15 at 2 μM alone after 24 h incubation.
Increased viability to approximately 0.6 when co-incubated with 100 μM DMP.
Increased viability to approximately 0.9 when co-incubated with 300 μM DMP.
Increased viability to approximately 0.75 when co-incubated with 100 μM DMSA.
Increased viability to approximately 0.8 when co-incubated with 150 μM DMSA.

Cell Viability Assay^[3]

Cell Line:

NB4 cells
Concentration:

0.6 μM, 1.2 μM, 2.4 μM, 3.6 μM; 0.6 μM with 50 μM BSO pre-treatment, 1.2 μM with 50 μM BSO pre-treatment, 2.4 μM with 50 μM BSO pre-treatment, 3.6 μM with 50 μM BSO pre-treatment
Incubation Time:

12 h, 24 h
Result:

Reduced NB4 cell viability to ~0.8 at 0.6 μM, ~0.6 at 1.2 μM, ~0.3 at 2.4 μM, and ~0.1 at 3.6 μM after 12 h incubation.
Reduced NB4 cell viability to ~0.8 at 0.6 μM, ~0.7 at 1.2 μM, ~0.4 at 2.4 μM, and ~0.2 at 3.6 μM after 24 h incubation.
Enhanced the viability-reducing effect with 50 μM BSO pre-treatment, resulting in viability of ~0.05 at 3.6 μM after 12 h incubation, and ~0.5 at 3.6 μM after 24 h incubation.

Chemical Information

CAS No. 256348-71-7
Molecular Weight 273.24
Formula C₉H₁₂AsNS₂
SMILES

S1[As](SCCC1)C2=CC=C(N)C=C2
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

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

Purity & Documentation

Handling Instructions (2659 KB)

References

[1]. Liu Y, et al. Dithiaarsanes induce oxidative stress-mediated apoptosis in HL-60 cells by selectively targeting thioredoxin reductase. Journal of medicinal chemistry. 2014 Jun 26;57(12):5203-11. [Content Brief]

[2]. Shi S, et al. Structure-Guided optimization of PAO-PDT yields TrxR inhibitors as potential anticancer agent. European journal of medicinal chemistry. 2026 Feb 05;303:118407. [Content Brief]

[3]. Fan XY, et al. A mitochondria-targeted organic arsenical accelerates mitochondrial metabolic disorder and function injury. Bioorganic & medicinal chemistry. 2019 Mar 01;27(5):760-768.

[4]. Song ZL, et al. Structural Modification of Aminophenylarsenoxides Generates Candidates for Leukemia Treatment Thioredoxin Reductase Inhibition. Journal of medicinal chemistry. 2021 Nov 11;64(21):16132-16146.

Calculators

Molarity Calculator

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

Mass Mass

Concentration Concentration

Volume Volume

Molecular Weight Molecular Weight

Dilution Calculator

Concentration _(start) × Volume _(start) = Concentration _(final) × Volume _(final)

Concentration _(start) Concentration _(start)

Volume _(start) Volume _(start)

Concentration _(final) Concentration _(final)

Volume _(final) Volume _(final)

Help & FAQs

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.

Product Name:
Cat. No.:
Quantity:
MCE Japan Authorized Agent:

Product Name:
CAS No.:
Species:
Purity:
Quantity:

PAO-PDT

All TrxR Isoforms