Cat. No.: HY-187653

DCZ3112

DCZ3112 is a Hsp90/Cdc37 protein-protein interaction inhibitor, with a K_d value of 4.98 µM against human Hsp90. DCZ3112 binds to the N-terminal domain of Hsp90, disrupts the Hsp90-Cdc37 interaction, and does not inhibit the ATPase activity of Hsp90. DCZ3112 induces G1 phase cell cycle arrest, apoptosis, reduces the phosphorylation levels of AKT and ERK, and inhibits the proliferation of HER2-positive breast cancer cells. DCZ3112 can be used in breast cancer-related research.

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

CAS No.: 2556837-25-1
Formula: C₁₅H₁₄ClF₃N₈
Molecular Weight:398.78

Storage:

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

DCZ3112 Chemical Structure

CAS No.: 2556837-25-1

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Use of MCE Products

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

Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Purity & Documentation
References
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Biological Activity

Description

IC₅₀ & Target^[1]^[2]^[3]

HSP90

4.98 μM (Kd)

Cdc37

ERK

Akt

All HSP Isoforms :

All Akt Isoforms :

All ERK Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
SK-BR-3	IC50	7.9 μM	Antiproliferative activity against human SK-BR-3 breast cancer cells assessed as reduction in cell viability incubated for 72 hrs by Sulforhodamine B (SRB) assay. Antiproliferative activity against human SK-BR-3 breast cancer cells assessed as reduction in cell viability incubated for 72 hrs by Sulforhodamine B (SRB) assay.	30017966
BT-474	IC50	4.6 μM	Antiproliferative activity against human BT-474 breast cancer cells assessed as reduction in cell viability incubated for 72 hrs by Sulforhodamine B (SRB) assay. Antiproliferative activity against human BT-474 breast cancer cells assessed as reduction in cell viability incubated for 72 hrs by Sulforhodamine B (SRB) assay.	30017966

In Vitro

DCZ3112 binds directly to recombinant full-length human Hsp90α, with a K_D value of 4.98 µM^[1].
DCZ3112 (20-40 µM; 12 h) reduces the protein levels of HER2, AKT and RAF-1 in BT-474 human breast cancer cells via post-transcriptional degradation rather than transcriptional inhibition^[1].
DCZ3112 (72 h) potently inhibits the proliferation of HER2-positive human breast cancer cells SK-BR-3 and BT-474 (with IC₅₀ values of 7.9 µM and 4.6 µM, respectively) as well as Geldanamycin (HY-15230)-resistant derivative cells, while it exhibits only extremely low activity against most HER2-negative human breast cancer cells^[1].
DCZ3112 (5-40 µM; 12 h) induces concentration-dependent degradation of the Hsp90 client proteins HER2, AKT, RAF-1, CDK4 and CDK6 in HER2-positive human breast cancer SK-BR-3 and BT-474 cells, exerts only weak effects in HER2-negative MDA-MB-231 cells, and does not induce Hsp72 upregulation^[1].
DCZ3112 (20 µM; 12 h) induces proteasome-dependent degradation of the Hsp90 client proteins HER2, AKT and RAF-1 in human breast cancer BT-474 cells^[1].
Combination treatment with DCZ3112 (72 h) and Trastuzumab (HY-P9907) or Pertuzumab (HY-P9912) exerts synergistic antiproliferative effects on HER2-positive SK-BR-3, BT-474, and Trastuzumab-resistant BT-474/T human breast cancer cells, with combination index (CI) values of all regimens being <1^[1].
Combination treatment with DCZ3112 (10 µM; 48 h) and 10 µg/mL Trastuzumab or Pertuzumab enhances the inhibitory effect on AKT and/or ERK phosphorylation in BT-474 human breast cancer cells compared with monotherapy^[1].
DCZ3112 (5-40 μM; 12 h) induces the degradation of Hsp90 client proteins EGFR, HER2 and AKT in Trastuzumab-resistant human breast cancer cell line BT-474/T, thereby overcoming Trastuzumab resistance mediated by EGFR upregulation^[1].
DCZ3112 selectively inhibits the growth of two HER2-positive breast cancer cell lines, SK-BR-3 and BT-474, with IC₅₀ values of 7.9 μM and 4.6 μM, respectively. It also blocks oncogenic signaling pathways and overcomes Trastuzumab resistance^[2].
DCZ3112 (20 µM; 24 h) induces G1-phase cell cycle arrest in HER2-positive human breast cancer cell lines SK-BR-3 and BT-474 by regulating G1-phase regulatory proteins^[1].
Combination treatment with DCZ3112 (15 µM; 48 h) and 10 µg/mL Trastuzumab enhances G1-phase cell cycle arrest in human breast cancer BT-474 cells, as compared with treatment with either agent alone^[1].
DC3112 (10-40 µM; 48 h) induces caspase-dependent apoptosis in HER2-positive SK-BR-3 and BT-474 human breast cancer cells, and triggers concentration-dependent cleavage of PARP, caspase-3, caspase-8 and caspase-9^[1].
Combination treatment with DCZ3112 (15 µM; 72 h) and 10 µg/mL Trastuzumab or Pertuzumab enhances the apoptosis-inducing effect on human breast cancer BT-474 cells compared with DCZ3112 monotherapy^[1].
DCZ3112 inhibits the interaction between Hsp90 and Cdc37, and potently suppresses the proliferation of two HER2-positive breast cancer cell lines, SK-BR-3 and BT-474, with IC₅₀ values of 7.9 μM and 4.6 μM, respectively. It also regulates the levels of Hsp90 client proteins and downstream signaling pathways^[3].

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

Western Blot Analysis^[1]

Cell Line:

SK-BR-3, BT-474, and MDA-MB-231 human breast cancer cells
Concentration:

5 µM; 10 µM; 20 µM; 40 µM
Incubation Time:

12 h
Result:

Downregulated Hsp90 client proteins HER2, AKT, RAF-1, CDK4, and CDK6 in a concentration-dependent manner in SK-BR-3 and BT-474 cells, and exerted weaker effects in HER2-negative MDA-MB-231 cells.
Showed no upregulation of Hsp72 (a hallmark of traditional Hsp90 inhibition).

Real Time qPCR^[1]

Cell Line:

BT-474 human breast cancer cells
Concentration:

20 µM; 40 µM
Incubation Time:

12 h
Result:

Did not inhibit transcription of HER2, AKT, or RAF-1 mRNA.

Cell Cycle Analysis^[1]

Cell Line:

SK-BR-3 and BT-474 human breast cancer cells
Concentration:

20 µM
Incubation Time:

24 h
Result:

Induced G1-phase cell-cycle arrest in SK-BR-3 and BT-474 cells, accompanied by downregulation of G1-related proteins P-Rb, CDK4, and Cyclin D1, and upregulation of P21.

Western Blot Analysis^[1]

Cell Line:

SK-BR-3 and BT-474 human breast cancer cells
Concentration:

10 µM; 20 µM; 40 µM
Incubation Time:

48 h
Result:

Induced a concentration-dependent increase in cleavage of PARP, caspase-3, caspase-8, and caspase-9 in SK-BR-3 and BT-474 cells.

Cell Cycle Analysis^[1]

Cell Line:

BT-474 human breast cancer cells
Concentration:

15 µM DCZ3112; 10 µg/mL Trastuzumab; 10 µg/mL Pertuzumab
Incubation Time:

48 h
Result:

Increased the percentage of G1-phase cells from 69.7% (DCZ3112 alone) or 69.9% (Trastuzumab alone) to 81.8% when combined with Trastuzumab; showed no significant enhancement when combined with Pertuzumab.

Apoptosis Analysis^[1]

Cell Line:

BT-474 human breast cancer cells
Concentration:

15 µM DCZ3112; 10 µg/mL Trastuzumab; 10 µg/mL Pertuzumab
Incubation Time:

72 h
Result:

Enhanced apoptosis induction when combined with Trastuzumab or Pertuzumab compared to DCZ3112 treatment alone, while neither Trastuzumab nor Pertuzumab alone induced detectable apoptosis.

Western Blot Analysis^[1]

Cell Line:

BT-474 human breast cancer cells
Concentration:

10 µM DCZ3112; 10 µg/mL Trastuzumab; 10 µg/mL Pertuzumab
Incubation Time:

48 h
Result:

Induced a greater reduction in AKT phosphorylation when combined with Trastuzumab or Pertuzumab compared to any agent alone; synergistically inhibited ERK phosphorylation when combined with Trastuzumab.

Western Blot Analysis^[1]

Cell Line:

Trastuzumab-resistant BT-474/T human breast cancer cells
Concentration:

5 µM; 10 µM; 20 µM; 40 µM
Incubation Time:

12 h
Result:

Decreased EGFR, HER2, and AKT protein levels in BT-474/T cells, similar to its effects in parental BT-474 cells.

In Vivo

DCZ3112 (70 mg/kg; i.p.; daily; 18 days) alone inhibits BT-474 breast cancer xenograft growth by 61% and exhibits enhanced synergistic antitumor activity when combined with Trastuzumab^[1].

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

Animal Model:

Balb/cA-nude (female, 5-6 weeks old)^[1]
Dosage:

70 mg/kg
Administration:

i.p.; daily; 18 days
Result:

Inhibited tumor growth by 61% (p < 0.01) on the final treatment day.
Decreased levels of Hsp90 client proteins HER2 and AKT in tumor tissue.
Produced enhanced antitumor efficacy (p < 0.05) when combined with Trastuzumab, including regression of one of six tumors.
Caused synergistic reduction in AKT and ERK phosphorylation in tumor tissues when combined with Trastuzumab.
Was rapidly detected in plasma and tumor tissue after a single 70-mg/kg i.p. dose, remained detectable for 24 hours, and suppressed HER2 and AKT levels in tumor tissue for at least 24 hours.
Was well tolerated with no significant body weight loss.

Chemical Information

CAS No. 2556837-25-1
Molecular Weight 398.78
Formula C₁₅H₁₄ClF₃N₈
SMILES

FC(F)(F)C1=CC(=CC=C1Cl)NC2=NC(=NN)N=C(N2)N3N=C(C=C3C)C
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]. Chen X, et al. DCZ3112, a novel Hsp90 inhibitor, exerts potent antitumor activity against HER2-positive breast cancer through disruption of Hsp90-Cdc37 interaction. Cancer Lett. 2018 Oct 10;434:70-80.

[2]. Kamel EM, et al. Disrupting the Hsp90-Cdc37 axis: a selective strategy for targeting oncogenic kinases in cancer. RSC advances. 2025 Jun 04;15(24):19376-19391.

[3]. Lu H, et al. Recent advances in the development of protein-protein interactions modulators: mechanisms and clinical trials. Signal Transduct Target Ther. 2020 Sep 23;5(1):213. [Content Brief]

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DCZ3112

All HSP Isoforms

All Akt Isoforms

All ERK Isoforms

Biological Activity

Chemical Information

Purity & Documentation

References

Calculators

Help & FAQs

DCZ3112 Related Classifications

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