Pipeline

Explore Our Pipeline

Investigational drugs mentioned are for use in clinical studies only, and may be studied alone or in combination with drugs for indications that have not been approved by the FDA. Approved drugs mentioned are also being studied for uses for which they are not approved. Safety and efficacy have not been established for any of these drugs for the uses being studied.

AbbVie in no way intends to recommend or imply that these drugs should be used for unapproved uses.

Hematologic Malignancies

Phase 1

Phase 2

Phase 3

Overview

Venetoclax (ABT-199/GDC-0199) is a selective, orally bioavailable small-molecule BCL-2 inhibitor.1

Proposed Mechanism of Disease

The BCL-2 protein binds and sequesters proapoptotic proteins, limiting their ability to initiate apoptosis. Venetoclax is designed to bind to BCL-2, preventing it from binding to proapoptotic proteins and thereby restoring the cell's ability to undergo apoptosis.1

Development

Venetoclax was approved in April 2016 under accelerated approval conditions for the treatment of patients with CLL with 17p deletion, as detected by an FDA-approved test, who have received at least one prior therapy. AbbVie and Genentech continue to investigate venetoclax in ongoing phase 3 and phase 2 clinical trials for the treatment of CLL, as well as a variety of other cancers, including acute myeloid leukemia (AML), multiple myeloma (MM), subtypes of non-Hodgkin lymphoma (NHL) [mantle cell lymphoma (MCL), Waldenstrom's macroglobulinemia (WM), diffuse large B-cell lymphoma (DLBCL), follicular lymphoma (FL)] and acute lymphoblastic leukemia (ALL).

Clinical Trials

View select clinical trials with venetoclax now. To view a full list of clinical trials in which venetoclax is being investigated, please visit ClinicalTrials.gov.

Venetoclax (ABT-199/GDC-0199) is an approved drug being studied for unapproved uses. Safety and efficacy have not been established for these unapproved uses.

VENETOCLAX MOD and PROPOSED MOA

See the role of the BCL-2 pathway in evading apoptosis and promoting tumor survival. Learn about venetoclax and its role in BCL-2 inhibition.

Chronic Lymphocytic Leukemia (CLL)

Multiple Myeloma (MM)

Acute Myeloid Leukemia (AML)

Non-Hodgkin Lymphoma (NHL)

Myelodysplastic Syndromes (MDS)

Overview

Navitoclax (ABT-263) is an orally active inhibitor of the BCL-XL and BCL-2 proteins.2

Proposed Mechanism of Disease

Inhibiting the JAK2 signaling network at both the initiating stage (JAK2) and the effector stage (BCL-XL/BCL-2) may reduce tumor burden while minimizing resistance to JAK-2 inhibition.3,4

Development

Navitoclax is in phase 2 development for myelofibrosis in combination with ruxolitinib.

Clinical Trials

View select clinical trials with navitoclax now. To view a full list of clinical trials in which navitoclax is being investigated, please visit ClinicalTrials.gov.

Navitoclax (ABT-263) is an investigational drug for clinical study only. Safety and efficacy have not been established.

Myelofibrosis (MF)

Overview

ABBV-621 is a Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL) receptor agonist.

Development

ABBV-621 is being studied in a phase 1 clinical trial in patients with previously treated solid tumors and hematologic malignancies.

Clinical Trials

View select clinical trials with ABBV-621 now. To view a full list of clinical trials in which ABBV-621 is being investigated, please visit ClinicalTrials.gov.

ABBV-621 is an investigational drug for clinical study only. Safety and efficacy have not been established.

Non-Hodgkin Lymphoma (NHL)

Acute Myeloid Leukemia (AML)

Overview

Mivebresib (ABBV-075) is an orally active small-molecule bromodomain (BRD) and extra-terminal motif (BET) inhibitor.5

Development

Mivebresib is being studied in a phase 1 clinical trial in patients with advanced hematologic malignancies, prostate cancer, and other solid tumors.

Clinical Trials

View select clinical trials with mivebresib now. To view a full list of clinical trials in which mivebresib is being investigated, please visit ClinicalTrials.gov.

Mivebresib (ABBV-075) is an investigational drug for clinical study only. Safety and efficacy have not been established.

Acute Myeloid Leukemia (AML)

Multiple Myeloma (MM)

Non-Hodgkin Lymphoma (NHL)

Overview

ABBV-744 is a bromodomain II (BDII)-selective bromodomain and extra-terminal domain (BET) protein inhibitor.

Proposed Mechanism of Disease

The BET family of proteins is characterized by the presence of 2 tandem bromodomains (BDI and BDII) and an extra-terminal domain.6 BET bromodomains recognize acetylated lysines on transcription factors and histones, facilitating transcription of key genes involved in tumorigenesis (eg, c-myc, androgen receptor).6,7 ABBV-744 binds with high selectivity to the BDII of BET proteins, thereby releasing the BET proteins and their cofactors from chromatin.6 Inhibition of BET proteins thus has the potential to suppress transcription of key genes involved in tumorigenesis.

Development

ABBV-744 is being studied in a phase 1 clinical trial in patients with metastatic castrate-resistant prostate cancer (mCRPC) and relapsed/refractory acute myeloid leukemia (AML).

Clinical Trials

View select clinical trials with ABBV-744 now. To view a full list of clinical trials in which ABBV-744 is being investigated, please visit ClinicalTrials.gov.

ABBV-744 is an investigational drug for clinical study only. Safety and efficacy have not been established.

Acute Myeloid Leukemia (AML)

Lung cancer

Phase 1

Phase 2

Phase 3

Overview

Veliparib (ABT-888) is an oral poly (adenosine diphosphate [ADP]-ribose) polymerase (PARP) inhibitor that AbbVie is evaluating in multiple tumor types.8,9

Proposed Mechanism of Action

Proteins of the PARP family are naturally occurring enzymes in human cells that are critical to the repair of single-strand DNA breaks.8,9 While this is a useful process to maintain the integrity of healthy cells, the same process can also repair chemotherapy-induced DNA damage in cancer cells that may have limited capacity for repairing double-strand DNA breaks.8,9 Veliparib is designed to inhibit PARP1 and PARP2, potentially leading to the accumulation of single-strand and double-strand DNA breaks in tumor cells that may have limited capacity for DNA repair, which results in chromosomal instability, cell cycle arrest, and subsequent apoptosis.8,9,11

Development

Veliparib is being developed in settings where it can be combined with common DNA-damaging therapies like chemotherapy or radiation.8,9,12-15 It is in clinical trials for the treatment of patients with BRCA-deficient breast cancer, ovarian cancer, and lung cancer, as well as a number of other cancer types.

Clinical Trials

View select clinical trials with veliparib now. To view a full list of clinical trials in which veliparib is being investigated, please visit ClinicalTrials.gov.

Veliparib (ABT-888) is an investigational drug that is for clinical study only. Safety and efficacy have not been established.

MOD and Proposed MOA

See how Veliparib may play a role in dual PARP inhibition.

Non-Squamous Non-Small Cell Lung Cancer (NsqNSCLC)

Small Cell Lung Cancer (SCLC)

Overview

Rovalpituzumab tesirine (Rova-T) is an antibody-drug conjugate (ADC) comprising a humanized DLL3-specific IgG1 monoclonal antibody conjugated to a pyrrolobenzodiazepine dimer (PBD), a sequence-selective DNA cross-linking agent.16

Proposed Mechanism of Action

DLL3 is expressed at high levels on the cell surface of >80% of small cell lung cancer (SCLC) and large cell neuroendocrine carcinoma (LCNEC) tumors, with little to no expression in normal tissues.16 In preclinical models, Rova-T has been shown to specifically bind to DLL3, followed by internalization and trafficking to late endosomes. The cytotoxin (PBD) is released, ultimately leading to apoptosis of the tumor cell with minimal effect on normal tissue.16

Development

Rova-T is currently being investigated in phase 1 through phase 3 trials for the treatment of SCLC and other advanced solid tumors. Rova-T has received orphan drug designation from the FDA for treatment of SCLC.

Clinical Trials

View select clinical trials with Rova-T now. To view a full list of clinical trials in which Rova-T is being investigated, please visit ClinicalTrials.gov.

Rovalpituzumab tesirine (Rova-T) is an investigational drug for clinical study only. Safety and efficacy have not been established.

MOD and Proposed MOA

Learn more about rovalpituzumab tesirine (Rova-T), an antibody-drug conjugate.

Small Cell Lung Cancer (SCLC)

Overview

Telisotuzumab vedotin (Teliso-V; ABBV-399) is a cMet-targeted antibody-drug conjugate (ADC).

Proposed Mechanism of Action

In preclinical models, Teliso-V delivers a potent cytotoxin to cMet-overexpressing tumor cells enabling cell killing regardless of reliance on MET signaling.17

Development

Teliso-V is being studied in a phase 2 clinical trial in patients with non-small cell lung cancer (NSCLC) and in a phase 1 trial in patients with solid tumors.

Clinical Trials

View select clinical trials with telisotuzumab vedotin now. To view a full list of clinical trials in which telisotuzumab vedotin is being investigated, please visit ClinicalTrials.gov.

Telisotuzumab vedotin (Teliso-V; ABBV-399) is an investigational drug for clinical study only. Safety and efficacy have not been established.

Non-Small Cell Lung Cancer (NSCLC)

Overview

ABBV-927 is a differentiated CD40 agonistic monoclonal antibody (mAb) selected for enhanced activation of myeloid-lineage cells (moDC) versus B cells.

Proposed Mechanism of Action

CD40 is the key costimulatory molecule that functions as a master switch for both the innate and adaptive immune systems. CD40 is expressed on antigen-presenting cells (APCs) such as dendritic cells, monocytes, macrophages, and B cells. An agonistic anti-CD40 antibody can achieve potent antitumor immunity through initiating antigen presentation, promoting adaptive immunity, and reprogramming a suppressive tumor microenvironment. The effect of CD40 agonism depends on the type of cell expressing CD40. CD40 agonism on dendritic cells increases their ability to process and present tumor-associated antigens to local cytotoxic T lymphocytes. CD40 agonism on macrophages can generate tumoricidal myeloid cells.18

Development

ABBV-927 is being studied in phase 1 trials for the treatment of advanced solid tumors as monotherapy or in combination with other agents. Expansion cohorts will evaluate ABBV-927 in patients with non-small cell lung cancer, squamous cell carcinoma of the head and neck, cutaneous melanoma, or pancreatic adenocarcinoma.

Clinical Trials

View select clinical trials with ABBV-927 now. To view a full list of clinical trials in which ABBV-927 is being investigated, please visit ClinicalTrials.gov.

ABBV-927 is an investigational drug for clinical study only. Safety and efficacy have not been established.

Non-Small Cell Lung Cancer

Breast cancer

Phase 1

Phase 2

Phase 3

Overview

Veliparib (ABT-888) is an oral poly (adenosine diphosphate [ADP]-ribose) polymerase (PARP) inhibitor that AbbVie is evaluating in multiple tumor types.8,9

Proposed Mechanism of Action

Proteins of the PARP family are naturally occurring enzymes in human cells that are critical to the repair of single-strand DNA breaks.8,9 While this is a useful process to maintain the integrity of healthy cells, the same process can also repair chemotherapy-induced DNA damage in cancer cells that may have limited capacity for repairing double-strand DNA breaks.9,10 Veliparib is designed to inhibit PARP1 and PARP2, potentially leading to the accumulation of single-strand and double-strand DNA breaks in tumor cells that may have limited capacity for DNA repair, which results in chromosomal instability, cell cycle arrest, and subsequent apoptosis.8,9,11

Development

Veliparib is being developed in settings where it can be combined with common DNA-damaging therapies like chemotherapy or radiation.8,9,12-15 It is in clinical trials for the treatment of patients with BRCA-deficient breast cancer, ovarian cancer, and lung cancer, as well as a number of other cancer types.

Clinical Trials

View select clinical trials with veliparib now. To view a full list of clinical trials in which veliparib is being investigated, please visit ClinicalTrials.gov.

Veliparib (ABT-888) is an investigational drug that is for clinical study only. Safety and efficacy have not been established.

MOD and Proposed MOA

See how veliparib may play a role in dual PARP inhibition.

BRCA-Deficient Breast Cancer

Solid Tumors

Phase 1

Phase 2

Phase 3

Overview

ABBV-621 is a Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL) receptor agonist.

Development

ABBV-621 is being studied in a phase 1 clinical trial in patients with previously treated solid tumors and hematologic malignancies.

Clinical Trials

View select clinical trials with ABBV-621 now. To view a full list of clinical trials in which ABBV-621 is being investigated, please visit ClinicalTrials.gov.

ABBV-621 is an investigational drug for clinical study only. Safety and efficacy have not been established.

Previously Treated Solid Tumors

Overview

Veliparib (ABT-888) is an oral poly (adenosine diphosphate [ADP]-ribose) polymerase (PARP) inhibitor that AbbVie is evaluating in multiple tumor types.8,9

Proposed Mechanism of Action

Proteins of the PARP family are naturally occurring enzymes in human cells that are critical to the repair of single-strand DNA breaks.8,9 While this is a useful process to maintain the integrity of healthy cells, the same process can also repair chemotherapy-induced DNA damage in cancer cells that may have limited capacity for repairing double-strand DNA breaks.9,10 Veliparib is designed to inhibit PARP1 and PARP2, potentially leading to the accumulation of single-strand and double-strand DNA breaks in tumor cells that may have limited capacity for DNA repair, which results in chromosomal instability, cell cycle arrest, and subsequent apoptosis.8,9,11

Development

Veliparib is being developed in settings where it can be combined with common DNA-damaging therapies like chemotherapy or radiation.8,9/a>,12-15 It is in clinical trials for the treatment of patients with BRCA-deficient breast cancer, ovarian cancer, and lung cancer, as well as a number of other cancer types.

Clinical Trials

View select clinical trials with veliparib now. To view a full list of clinical trials in which veliparib is being investigated, please visit ClinicalTrials.gov.

Veliparib (ABT-888) is an investigational drug that is for clinical study only. Safety and efficacy have not been established.

MOD and Proposed MOA

See how veliparib may play a role in dual PARP inhibition.

Ovarian Cancer

Overview

Mivebresib (ABBV-075) is an orally active small-molecule bromodomain (BRD) and extra-terminal motif (BET) inhibitor.5

Development

Mivebresib is being studied in a phase 1 clinical trial in patients with advanced hematologic malignancies, prostate cancer, and other solid tumors.

Clinical Trials

View select clinical trials with mivebresib now. To view a full list of clinical trials in which mivebresib is being investigated, please visit ClinicalTrials.gov.

Mivebresib (ABBV-075) is an investigational drug for clinical study only. Safety and efficacy have not been established.

Prostate Cancer

Advanced Cancers

Overview

Telisotuzumab vedotin (Teliso-V; ABBV-399) is a cMet-targeted antibody-drug conjugate (ADC).

Proposed Mechanism of Action

In preclinical models, Teliso-V delivers a potent cytotoxin to cMet-overexpressing tumor cells enabling cell killing regardless of reliance on MET signaling.17

Development

Teliso-V is being studied in a phase 2 clinical trial in patients with non-small cell lung cancer (NSCLC) and in a phase 1 trial in patients with solid tumors.

Clinical Trials

View select clinical trials with telisotuzumab vedotin now. To view a full list of clinical trials in which telisotuzumab vedotin is being investigated, please visit ClinicalTrials.gov.

Telisotuzumab vedotin (Teliso-V; ABBV-399) is an investigational drug for clinical study only. Safety and efficacy have not been established.

Solid Tumors

Overview

ABBV-085 is a tumor antigen LRRC15-targeted antibody-drug conjugate (ADC).

Proposed Mechanism of Action

LRRC15 is frequently overexpressed in multiple tumor types.16 As an ADC, ABBV-085 is designed to remain stable in the bloodstream, potentially releasing the potent cytotoxin only inside targeted cancer cells.

Development

ABBV-085 is being studied in a phase 1 clinical trial in patients with advanced solid tumors.

Clinical Trials

To view a full list of clinical trials in which ABBV-085 is being investigated, please visit ClinicalTrials.gov.

ABBV-085 is an investigational drug for clinical study only. Safety and efficacy have not been established.

Advanced Solid Tumors

Overview

ABBV-321 is an epidermal growth factor receptor (EGFR)-targeted antibody-drug conjugate (ADC).

Proposed Mechanism of Action

ABBV-321 is our third-generation EGFR ADC that has three important distinctions from ABT-414. First, it contains an affinity-matured antibody (ABT-806 AM1) with a higher affinity for EGFR. Second and third, it utilizes a different linker that attaches a highly potent cytotoxic agent called a pyrrolobenzodiazepine (PBD) dimer with a fixed DAR of 2.0. PBDs are considered more potent than the auristaten conjugates. ABBV-321 is thought to remain stable in the bloodstream, potentially releasing the potent chemotherapy agent only inside targeted cancer cells. Studies are being conducted to determine if this approach could help reduce the toxic side effects of traditional chemotherapy while potentially enhancing antitumor activity.

Development

Being developed by AbbVie researchers, ABBV-321 is currently being investigated in a phase 1 study for the treatment of patients with advanced solid tumors associated with overexpression of the epidermal growth factor receptor (EGFR) or its ligands.

Clinical Trials

To view a full list of clinical trials in which ABBV-321 is being investigated, please visit ClinicalTrials.gov.

ABBV-321 is an investigational drug for clinical study only. Safety and efficacy have not been established.

Advanced Solid Tumors

Overview

Rovalpituzumab tesirine (Rova-T) is an antibody-drug conjugate (ADC) comprising a humanized DLL3-specific IgG1 monoclonal antibody conjugated to a pyrrolobenzodiazepine dimer (PBD), a sequence-selective DNA cross-linking agent.16

Proposed Mechanism of Action

DLL3 is expressed at high levels on the cell surface of >80% of small cell lung cancer (SCLC) tumors, with little to no expression in normal tissues.16 In preclinical models, Rova-T has been shown to specifically bind to DLL3, followed by internalization and trafficking to late endosomes. The cytotoxin (PBD) is released, ultimately leading to apoptosis of the tumor cell with minimal effect on normal tissue.16

Development

Rova-T is currently being investigated in phase 1 through phase 3 trials for the treatment of SCLC and other advanced solid tumors. Rova-T has received orphan drug designation from the FDA for treatment of SCLC.

Rovalpituzumab tesirine (Rova-T) is an investigational drug for clinical study only. Safety and efficacy have not been established.

MOD and Proposed MOA

Learn more about rovalpituzumab tesirine (Rova-T), an antibody-drug conjugate.

Advanced Solid Tumors

Overview

ABT-165 is a dual variable domain (DVD) immunoglobulin (bispecific antibody) that inhibits both DLL4 and VEGF.19

Development

ABT-165 is being studied in phase 1 trials for the treatment of patients with advanced solid tumors.

Clinical Trials

View select clinical trials with ABT-165 now. To view a full list of clinical trials in which ABT-165 is being investigated, please visit ClinicalTrials.gov.

ABT-165 is an investigational drug for clinical study only. Safety and efficacy have not been established.

Solid Tumors

Overview

ABBV-181 is a monoclonal antibody antagonist against PD1.

Proposed Mechanism of Disease

Programmed cell death-1 (PD1)/programmed cell death ligand-1 (PD-L1) interactions are part of an immune system checkpoint pathway that prevents T cells from causing damage to healthy cells. Tumor cells often overexpress PD-L1 to take advantage of this checkpoint and prevent an antitumor immune response.20 ABBV-181 blocks the interaction between PD-1 and its 2 ligands, PD-L1 and PD-L2, by binding to PD1. This prevents the inhibitory signaling pathway from being triggered when T cells encounter the tumor and restores the immune system's ability to recognize tumor cells as abnormal. T cells can then target these tumor cells for death.

Development

ABBV-181 is being studied in phase 1 trials for the treatment of advanced solid tumors in combination with other agents.

Clinical Trials

View select clinical trials with ABBV-181 now. To view a full list of clinical trials in which ABBV-181 is being investigated, please visit ClinicalTrials.gov.

ABBV-181 is an investigational drug for clinical study only. Safety and efficacy have not been established.

Advanced Solid Tumors

Overview

ABBV-368 is an OX40 agonistic monoclonal antibody with differentiated properties.

Proposed Mechanism of Disease

OX40 is a TNF-receptor family member that is expressed on activated CD4+ and CD8+ T cells. OX40 is a costimulator of antigen-specific T-cell activation that is transiently upregulated after antigen stimulation. It is also constitutively expressed on activated regulatory T cells within the tumor. An OX40 agonist acts to prolong activation and subsequent differentiation of antitumor T cells and inhibits the function of T regulatory cells (Tregs) in the tumor microenvironment.21 ABBV-368 is an anti-OX40 mAb with ligand-like activity. Binding of ABBV-368 to OX40 may activate T-cell signaling and suppress Treg function.

Development

ABBV-368 is being studied in phase 1 trials for the treatment of locally advanced or metastatic solid tumors as monotherapy or in combination with other agents.

Clinical Trials

View select clinical trials with ABBV-368 now. To view a full list of clinical trials in which ABBV-368 is being investigated, please visit ClinicalTrials.gov.

ABBV-368 is an investigational drug for clinical study only. Safety and efficacy have not been established.

Advanced Solid Tumors

Overview

ABBV-927 is a differentiated CD40 agonistic mAb selected for enhanced activation of myeloid-lineage cells (moDC) versus B cells.

Proposed Mechanism of Disease

CD40 is the key costimulatory molecule that functions as a master switch for both the innate and adaptive immune systems. CD40 is expressed on antigen-presenting cells (APCs) such as dendritic cells, monocytes, macrophages, and B cells. An agonistic anti-CD40 antibody can achieve potent anti-tumor immunity through initiating antigen presentation, promoting adaptive immunity, and reprogramming a suppressive tumor microenvironment. The effect of CD40 agonism depends on the type of cell expressing CD40. CD40 agonism on dendritic cells increases their ability to process and present tumor-associated antigens to local cytotoxic T lymphocytes. CD40 agonism on macrophages can generate tumoricidal myeloid cells.18 ABBV-927 is an agonistic CD40 mAb that was selected for potency on myeloid-lineage cells.

Development

ABBV-927 is being studied in phase 1 trials for the treatment of advanced solid tumors as monotherapy or in combination with other agents. Expansion cohorts will evaluate ABBV-927 in patients with non-small cell lung cancer, squamous cell carcinoma of the head and neck, cutaneous melanoma, or pancreatic adenocarcinoma.

Clinical Trials

View select clinical trials with ABBV-927 now. To view a full list of clinical trials in which ABBV-927 is being investigated, please visit ClinicalTrials.gov.

ABBV-927 is an investigational drug for clinical study only. Safety and efficacy have not been established.

Advanced Solid Tumors

Overview

ABBV-744 is a bromodomain II (BDII)-selective bromodomain and extra-terminal domain (BET) protein inhibitor.

Proposed Mechanism of Disease

The BET family of proteins is characterized by the presence of 2 tandem bromodomains (BDI and BDII) and an extra-terminal domain.6 BET bromodomains recognize acetylated lysines on transcription factors and histones, facilitating transcription of key genes involved in tumorigenesis (eg, c-myc, androgen receptor).6,7 ABBV-744 binds with high selectivity to the BDII of BET proteins, thereby releasing the BET proteins and their cofactors from chromatin.6 Inhibition of BET proteins thus has the potential to suppress transcription of key genes involved in tumorigenesis.

Development

ABBV-744 is being studied in a phase 1 clinical trial in patients with metastatic castrate-resistant prostate cancer (mCRPC) and relapsed/refractory acute myeloid leukemia (AML).

Clinical Trials

View select clinical trials with ABBV-744 now. To view a full list of clinical trials in which ABBV-744 is being investigated, please visit ClinicalTrials.gov.

ABBV-744 is an investigational drug for clinical study only. Safety and efficacy have not been established.

Metastatic Castrate-Resistant Prostate Cancer (mCRPC)

  1. Souers AJ, Leverson JD, Boghaert ER, et al. ABT-199, a potent and selective BCL-2 inhibitor, achieves antitumor activity while sparing platelets. Nat Med. 2013;19(2):202-208.
  2. Tse C, Shoemaker AR, Adickes J, et al. ABT-263: a potent and orally bioavailable Bcl-2 family inhibitor. Cancer Res. 2008;68(9):3421-3428.
  3. Waibel M, Solomon VS, Knight DA, et al. Combined targeting of JAK2 and Bcl-2/Bcl-xL to cure mutant JAK2-driven malignancies and overcome acquired resistance to JAK2 inhibitors. Cell Rep. 2013;5(4):1047-1059.
  4. Zhang M, Mathews Griner LA, Ju W, et al. Selective targeting of JAK/STAT signaling is potentiated by Bcl-xL blockade in IL-2-dependent adult T-cell leukemia. Proc Natl Acad Sci U S A. 2015;112(40):12480-12485.
  5. McDaniel KF, Wang L, Soltwedel T, et al. Discovery of N-(4-(2,4-Difluorophenoxy)-3-(6-methyl-7-oxo-6,7-dihydro-1H-pyrrolo[2,3-c]pyridin-4-yl)phenyl) ethanesulfonamide (ABBV-075/Mivebresib), a potent and orally available bromodomain and extraterminal domain (BET) family bromodomain inhibitor. J Med Chem. 2017;60(20):8369-8384.
  6. Xu Y, Vakoc CR. Targeting cancer cells with BET bromodomain inhibitors. Cold Spring Harb Perspect Med. 2017;7(7):a026674.
  7. Delmore JE, Issa GC, Lemieux ME, et al. BET bromodomain inhibition as a therapeutic strategy to target c-Myc. Cell. 2011;146(6):904-917.
  8. Donawho CK, Luo Y, Luo Y, et al. ABT-888, an orally active poly(ADP-ribose) polymerase inhibitor that potentiates DNA-damaging agents in preclinical tumor models. Clin Cancer Res. 2007;13(9):2728-2737.
  9. Palma JP, Wang YC, Rodriguez LE, et al. ABT-888 confers broad in vivo activity in combination with temozolomide in diverse tumors. Clin Cancer Res. 2009;15(23):7277-7290.
  10. Anders CK, Winer EP, Ford JM, et al. Poly(ADP-ribose) polymerase inhibition: "targeted" therapy for triple-negative breast cancer. Clin Cancer Res. 2010;16(19):4702-4710.
  11. Plummer ER, Calvert H. Targeting poly(ADP-ribose) polymerase: a two-armed strategy for cancer therapy. Clin Cancer Res. 2007;13(21):6252-6256.
  12. Owonikoko TK, Zhang G, Deng X, et al. Poly (ADP) ribose polymerase enzyme inhibitor, veliparib, potentiates chemotherapy and radiation in vitro and in vivo in small cell lung cancer. Cancer Med. 2014;3(6):1579-1594.
  13. Cheng H, Zhang Z, Borczuk A, et al. PARP inhibition selectively increases sensitivity to cisplatin in ERCC1-low non-small cell lung cancer cells. Carcinogenesis. 2013;34(4):739-749.
  14. Kummar S, Wade JL, Oza AM, et al. Randomized phase II trial of cyclophosphamide and the oral poly (ADP-ribose) polymerase inhibitor veliparib in patients with recurrent, advanced triple-negative breast cancer. Invest New Drugs. 2016 Mar 21. [Epub ahead of print]
  15. Reiss KA, Herman JM, Zahurak M, et al. A phase I study of veliparib (ABT-888) in combination with low-dose fractionated whole abdominal radiation therapy in patients with advanced solid malignancies and peritoneal carcinomatosis. Clin Cancer Res. 2015;21(1):68-76.
  16. Saunders LR, Bankovich AJ, Anderson WC, et al. A DLL3-targeted antibody-drug conjugate eradicates high-grade pulmonary neuroendocrine tumor-initiating cells in vivo. Sci Transl Med. 2015;7(302):302ra136.
  17. Wang J, Anderson MG, Oleksijew A, et al. ABBV-399, a c-Met antibody-drug conjugate that targets both MET-amplified and c-Met-overexpressing tumors, irrespective of MET pathway dependence. Clin Cancer Res. 2017 Feb 15;23(4):992-1000.
  18. Vonderheide RH, Glennie MJ. Agonistic CD40 antibodies and cancer therapy. Clin Cancer Res. 2013;19(5):1035-1043.
  19. Reynolds, PA, Smolen GA, Palmer RE, et al. Identification of a DNA-binding site and transcriptional target for the EWS-WT1(+KTS) oncoprotein. Genes Dev. 2003;17(17):2094-2107.
  20. Li Y, Hickson J, Ambrosi D, et al. ABT-165 is a first-in-class therapeutic dual variable domain immunoglobulin (DVD-IgTM) that targets DLL4 and VEGF for the treatment of cancer. Proceedings of the AACR, Part A: Abstracts 1-2696. 2016;57:abstract 867.
  21. Curti BD, Kovacsovics-Bankowski M, Morris N, et al. OX40 is a potent immune-stimulating target in late-stage cancer patients. Cancer Res. 2013;73(24):7189-7198.

Need more information?

Explore Careers

Contact Medical Information

For All Other Information