IP Library Patent Application 15541012
Patent Application
App. No. 15/541,012

HDAC1,2 INHIBITORS AND METHODS OF USING THE SAME

Loading inventors, assignments & file history…
Monitor This Case
Get email alerts when status or documents change.
Order Certified Copies
Most orders are placed with the USPTO same day — all within 24 business hours.
Order via The Patent Place →
Pre-filled with this patent's details
Quick Facts
Patent No.
US None
App. No.
15/541,012
Abstract

Disclosed herein are methods for treating a cancer and a method for sensitizing a cancer to a chemotherapeutic agent. Each method administers an agent that selectively inhibits HDAC1 and HDAC2 to a subject in need thereof. Also disclosed herein are methods for determining if a cancer is sensitive to an agent that selectively inhibits HDAC1 and HDAC2 and methods for monitoring the efficacy of a treatment for a cancer that includes administration of an agent that selectively inhibits HDAC1 and HDAC2.

Claims (25)

1 . A method of treating a cancer characterized by BCR-ABL expression or BBAP overexpression in a subject in need thereof, the method comprising administering to the subject an agent that selectively inhibits HDAC1 and HDAC2.

2 . The method of claim 1 , wherein the cancer is a B cell malignancy.

3 . The method of claim 2 , wherein the B cell malignancy is diffuse large B cell lymphoma or early Pre-B cell derived acute lymphoblastic leukemia (Pre-B-ALL).

4 . The method of claim 3 , wherein the diffuse large B cell lymphoma contains a gain-of-function mutation in Enhancer of Zeste Homologue 2 (EZH2), a gain-of-function mutation in a histone H3K27 methyltransferase, or a loss-of-function mutation in a H3K27 demethylase.

5 . The method of claim 3 , wherein the Pre-B-ALL contains a chromosomal translocation and wherein the chromosomal translocation is t(9;22).

6 . The method of claim 1 , wherein the cancer is further characterized as being dependent upon on a double-stranded break repair pathway.

7 . The method of claim 6 , wherein the double-stranded break repair pathway includes one or more of the group consisting of FEN1, EPC2, BAF180, and DNA Ligase I.

8 . The method of claim 1 , wherein the cancer is further characterized by increased H3K27me3.

9 . The method of claim 1 , further comprising determining if the cancer is characterized by BCR-ABL expression or BBAP overexpression,

wherein determining comprises detecting a level of BCR-ABL, a level of BBAP, or a level of BCR-ABL and a level of BBAP in a sample obtained from the subject, and comparing the detected levels of BCR-ABL, BBAP, or BCR-ABL and BBAP to levels of BCR-ABL, BBAP, or BCR-ABL and BBAP in a control sample, wherein if the detected level of BCR-ABL is increased relative to the control level of BCR-ABL, the cancer is characterized by BCR-ABL expression, and wherein if the detected level of BBAP is increased relative to the control level of BBAP, the cancer is characterized by BBAP overexpression.

10 . (canceled)

11 . (canceled)

12 . (canceled)

13 . The method of claim 1 , further comprising administering doxorubicin to the subject.

14 . A method of sensitizing a cancer characterized by BCR-ABL expression or BBAP overexpression to a chemotherapeutic agent in a subject in need thereof, the method comprising administering an agent that selectively inhibits HDAC1 and HDAC2 to the subject.

15 . The method of claim 14 , wherein the cancer is a B cell malignancy.

16 . The method of claim 15 , wherein the B cell malignancy is diffuse large B cell lymphoma or early Pre-B cell derived acute lymphoblastic leukemia (Pre-B-ALL).

17 . The method of claim 16 , wherein the diffuse large B cell lymphoma contains a gain-of-function mutation in Enhancer of Zeste Homologue 2 (EZH2), a gain-of-function mutation in a histone H3K27 methyltransferase, or a loss-of-function mutation in a H3K27 demethylase.

18 . The method of claim 16 , wherein the Pre-B-ALL contains a chromosomal translocation and wherein the chromosomal translocation is t(9;22).

19 . The method of claim 14 , wherein the cancer is further characterized as being dependent upon on a double-stranded break repair pathway.

20 . The method of claim 19 , wherein the double-stranded break repair pathway includes one or more of the group consisting of FEN1, EPC2, BAF180, and DNA Ligase I.

21 . The method of claim 14 , wherein the cancer is further characterized by increased H3K27me3.

22 . The method of claim 14 , further comprising determining if the cancer is characterized by BCR-ABL expression or BBAP overexpression,

wherein determining comprises detecting a level of BCR-ABL, a level of BBAP, or a level of BCR-ABL and a level of BBAP in a sample obtained from the subject, and comparing the detected levels of BCR-ABL, BBAP, or BCR-ABL and BBAP to levels of BCR-ABL, BBAP, or BCR-ABL and BBAP in a control sample, wherein if the detected level of BCR-ABL is increased relative to the control level of BCR-ABL, the cancer is characterized by BCR-ABL expression, and wherein if the detected level of BBAP is increased relative to the control level of BBAP, the cancer is characterized by BBAP overexpression.

23 - 44 . (canceled)

Assignments (4)
CONFIRMATORY LICENSE Recorded Sep 13, 2021
From: UNIVERSITY OF UTAH
To: NATIONAL INSTITUTES OF HEALTH (NIH), U.S. DEPT. OF HEALTH AND HUMAN SERVICES (DHHS), U.S. GOVERNMENT
Reel/Frame 057493/0332 →
CONFIRMATORY LICENSE Recorded Jun 18, 2019
From: UNIVERSITY OF UTAH
To: NATIONAL INSTITUTES OF HEALTH
Reel/Frame 049498/0373 →
ASSIGNMENT OF ASSIGNOR'S INTEREST Recorded Feb 11, 2019
From: BHASKARA, SRIVIDYA
To: UNIVERSITY OF UTAH
Reel/Frame 048298/0028 →
ASSIGNMENT OF ASSIGNOR'S INTEREST Recorded Feb 11, 2019
From: UNIVERSITY OF UTAH
To: UNIVERSITY OF UTAH RESEARCH FOUNDATION
Reel/Frame 048298/0128 →