CDK1 inhibitors(Cyclin-dependent kinase 1 inhibitors), CDK2 inhibitors(Cyclin-dependent kinase 2 inhibitors), CDK5 inhibitors(Cyclin-dependent kinase 5 inhibitors)

Therapeutic Areas

NeoplasmsImmune System DiseasesHemic and Lymphatic Diseases+ [2]

Active Indication-

Inactive Indication

Acute Lymphoblastic LeukemiaAcute Myeloid LeukemiaAdvanced breast cancer+ [12]

Originator Organization

Merck & Co., Inc.

Active Organization-

Inactive Organization

Merck Sharp & Dohme Corp.

AbbVie, Inc.Merck Sharp & Dohme LLC

Drug Highest PhaseDiscontinuedPhase 3

First Approval Date-

RegulationOrphan Drug (United States), Orphan Drug (European Union)

Structure/Sequence

Molecular FormulaC21H28N6O2

InChIKeyPIMQWRZWLQKKBJ-SFHVURJKSA-N

CAS Registry779353-01-4

Clinical Trials associated with Dinaciclib

NCT03484520

/ TerminatedPhase 1

Phase 1b Study of Venetoclax and Dinaciclib (MK7965) in Patients With Relapsed/Refractory Acute Myeloid Leukemia

An open-label, dose-escalation study to assess safety, pharmacokinetics and efficacy as well as determine the recommended Phase 2 doses of co-administered therapy of dinaciclib and venetoclax for patients with relapsed or refractory Acute Myeloid Leukemia (R/R AML).

Start Date23 Jul 2018

Sponsor / Collaborator

AbbVie, Inc.

[+1]

NCT01676753

/ CompletedPhase 1IIT

A Phase 1b Trial of the Cyclin-dependent Kinase Inhibitor Dinaciclib in Combination With Pembrolizumab in Patients With Advanced Breast Cancer and Assessment of MYC Oncogene Overexpression

The purpose of this trial is to determine the safety and tolerability (maximum tolerated dose (MTD)) of weekly dinaciclib in combination with pembrolizumab in patients with advanced breast cancer. Once this is defined, dose expansion will be performed at this MTD in patients with metastatic or locally advanced and unresectable triple negative breast cancer, to evaluate the efficacy of combined dinaciclib and pembrolizumab.

Start Date28 Dec 2016

Sponsor / Collaborator

The University of California, San Francisco

[+1]

NCT02684617

/ TerminatedPhase 1

Phase Ib Trial of Pembrolizumab (MK-3475) in Combination With Dinaciclib (MK-7965) in Subjects With Hematologic Malignancies (KEYNOTE-155).

The purpose of this study is to evaluate the safety and efficacy of pembrolizumab (MK-3475) used in combination with dinaciclib (MK-7965) in the treatment of relapsed or refractory chronic lymphocytic leukemia (rrCLL), multiple myeloma (rrMM), or diffuse large B-cell lymphoma (rrDLBCL).

Start Date29 Mar 2016

Sponsor / Collaborator

Merck Sharp & Dohme LLC

100 Clinical Results associated with Dinaciclib

100 Translational Medicine associated with Dinaciclib

100 Patents (Medical) associated with Dinaciclib

460

Literatures (Medical) associated with Dinaciclib

01 Aug 2025·COMPUTATIONAL BIOLOGY AND CHEMISTRY

Phytoflavonoids as alternative therapeutic effect for melanoma: Integrative Network pharmacology, molecular dynamics and drug-likeness profiling for lead discovery

Article

Author: Mittal, Abhilasha ; Prajapati, Manoj Kumar ; Panda, Pritipadma

Melanoma, an aggressive skin cancer, poses significant therapeutic challenges due to its resistance to conventional therapies and high metastatic potential. From this perspective, phytoflavonoids from different medicinal and aromatic plants gained attention due to their diverse multimodal anticancer effects with higher antioxidant and anti-inflammatory properties. This study explores phytoflavonoid potency against melanoma via a computer-aided drug design (CADD) platform. Using the core moiety of flavonoids (flavan), four most putative targets, such as cyclin-dependent kinases 1 and 5 (CDK1, CDK5), cell division cycles 25B and 225 C (CDC25B, and CDC225C), have been identified through a network pharmacology approach using TNMplot datasets (GenChip and RNA sequence). Further, 44 phytoflavonoids were selected from extensive literature, and molecular docking studies were carried out against four targets along with standard drugs using AutoDock 4.2 software. Subsequently, physicochemical, toxicity, pharmacokinetics, and drug-ability profiles of phytoflavonoids were predicted. Based on potency and drug-ability, we have selected 'CDK1-naringenin' with the standard drug complex, 'CDK1-dinaciclib,' for molecular dynamic simulation at 100 nanoseconds using GROMACS 2020 software. Based on potency (average docking score: 8.35 kcal/mol.), physicochemical properties (obeyed Lipinski rule of five), toxicity (class-IV), fifty percent lethal dose (2000 mg/kg), bioavailability (0.55), drug-likeness score (0.82), along with ideal pharmacokinetics profiles and higher protein-ligand stability, naringenin is considered as a potential and non-toxic anticancer candidate to be used for melanoma as alternative or complementary agent. The integrative and systematic analyses not only highlight the potential of phytoflavonoids but also select the potential lead from the library within limited resources to accelerate the current anticancer drug discovery process.

01 Mar 2025·MOLECULAR CELL

SLFN11-mediated ribosome biogenesis impairment induces TP53-independent apoptosis

Article

Author: Watanabe, Soyoka ; Kitajima, Shojiro ; Natsumeda, Manabu ; Yamamoto, Gaku ; Murai, Junko ; Tate, Sota ; Taniyama, Daiki ; Ogawa, Akane ; Nagahama, Masami ; Mori, Masaru ; Ohashi, Akihiro ; Izumikawa, Keiichi ; Fujiwara, Kohei ; Isoyama, Sho ; Kobayashi, Junya ; Higashiyama, Shigeki ; Sasanuma, Hiroyuki ; Morita, Tomoko Yamamori ; Tanaka, Soichiro ; Pommier, Yves ; Onji, Hiroshi ; Dan, Shingo ; Ohga, Takayuki ; Kageyama, Shun-Ichiro ; Okada, Masayasu ; Jo, Ukhyun ; Saito, Hitoshi

Impairment of ribosome biogenesis (RiBi) triggered by inhibition of ribosomal RNA (rRNA) synthesis and processing leads to various biological effects. We report that Schlafen 11 (SLFN11) induces TP53-independent apoptosis through RiBi impairment. Upon replication stress, SLFN11 inhibits rRNA synthesis with RNA polymerase I accumulation and increased chromatin accessibility in the ribosomal DNA (rDNA) genes. SLFN11-dependent RiBi impairment preferentially depletes short-lived proteins, particularly MCL1, leading to apoptosis in response to replication stress. SLFN11's Walker B motif (E669), DNA-binding site (K652), dephosphorylation site for single-strand DNA binding (S753), and RNase sites (E209/E214) are all required for the SLFN11-mediated RiBi impairment. Comparable effects were obtained with direct RNA polymerase I inhibitors and other RiBi inhibitory conditions regardless of SLFN11. These findings were extended across 34 diverse human cancer cell lines. Thus, we demonstrate that RiBi impairment is a robust inactivator of MCL1 and an additional proapoptotic mechanism by which SLFN11 sensitizes cancer cells to chemotherapeutic agents.

01 Feb 2025·Advanced Science

Targeting CDK2 Confers Vulnerability to Lenvatinib Via Driving Senescence in Anaplastic Thyroid Cancer

Article

Author: Ma, Ben ; Xiang, Jun ; Ji, Qinghai ; Qu, Ning ; Sang, Youzhou ; Yin, Min ; Ji, Dongmei ; Lu, Jiayi ; Wang, Yunjun ; Xu, Weibo ; Zhang, Yanzhi ; Liao, Tian ; Zhang, Jiwei ; Shi, Rongliang ; Wang, Yu ; Liu, Wanlin ; Guan, Qing ; Wang, Yuting ; Du, Xiaoxue

Abstract:

Anaplastic thyroid cancer (ATC) is the most lethal tumor arising from thyroid follicular epithelium. Lenvatinib is an off‐label use option for ATC patients in many countries but an approved prescription in Japan. However, lenvatinib resistance is a substantial clinical challenge. Clinical ATC samples including lenvatinib‐resistant tumors are used to build patient‐derived cells and patient‐derived xenografts. High‐throughput drug screening and synergy analyses are performed to identify an effective combination partner for lenvatinib. Cellular functions are detected by cell senescence, apoptosis, cell cycle, cell viability and colony formation assays. CDK2 inhibition showed the significant synthetic lethality with lenvatinib via inhibiting G1/S transition and inducing cell senescence in ATC. High expression of CDK2 is associated with lenvatinib resistance and poor clinical outcomes of ATC patients. Lenvatinib increased protein expression of CDK2 in lenvatinib‐resistant ATC cells. Mechanistically, lenvatinib inhibited protein degradation of CDK2 via reducing CDK2's interaction with the RACK1‐FBW7 complex, which is involved in ubiquitination and subsequent proteasomal degradation of CDK2. Combination of CDK2 inhibitors in clinical trials (Dinaciclib or PF‐07104091) and lenvatinib markedly suppressed growth of xenograft tumors from the lenvatinib‐resistant patient. The findings support the combination therapy strategy of lenvatinib and CDK2 inhibitor for lenvatinib‐resistant ATC patients with high CDK2 expression.

News (Medical) associated with Dinaciclib

11 Apr 2024

·www.sciencedaily.com

Scientists uncover key resistance mechanism to Wnt inhibitors in pancreatic and colorectal cancers

A new study reveals why some pancreatic and colorectal tumors resist targeted anti-Wnt drugs and suggests how to overcome it, offering new hope to patients with fully treatment-resistant cancers. Scientists at Duke-NUS Medical School have uncovered why some pancreatic and colorectal cancers[1] fail to respond to Wnt inhibitors, a promising new class of cancer drugs currently under development for these cancers. Their discovery, published in Science Advances, not only offers a new cancer therapy target but also a potential screening tool to identify those patients who will not benefit from this new therapy once it becomes available. Many gastrointestinal cancers grow uncontrollably when a mutation sets a key biological pathway that governs cell growth, called Wnt, on hyperdrive. The Wnt pathway is hijacked in this way in more than 80 per cent of colorectal cancers and some pancreatic cancers, driving rampant tumour growth. For this group of patients, drugs that block the Wnt pathway, known as Wnt inhibitors, hold great promise and they have been at the centre of intense scientific study, including at Duke-NUS[2]. "Although Wnt inhibitors have shown some promise in certain patients, our study reveals intrinsic resistance in others," said Dr Zhong Zheng, who led the study as a postdoctoral fellow at Duke-NUS' Cancer & Stem Cell Biology Programme. "Understanding the mechanisms behind this resistance is crucial for personalised treatments for patients when the drugs don't slow tumour growth at all." Focusing on colorectal and pancreatic cancers with a hyperactive Wnt pathway, Dr Zhong, together with Professor David Virshup who leads the Programme at Duke-NUS, used their Wnt inhibiting drug ETC-159, whose efficacy had been established in preclinical models, to assess the cancer cells' responsiveness. By analysing genetics data on both responsive and non-responsive tumours, they discovered that a second mutation in another gene, known as FBXW7, makes cancer cells stubbornly resistant to Wnt-blocking drugs. FBXW7 mutations occur in about 15 per cent of colorectal cancers. "The FBXW7 mutations change the personality of the cancer," explained Dr Zhong. "They no longer 'care' about the Wnt pathway and so the drugs no longer can do their work." Testing tumours for the FBXW7 genetic mutations could spare many patients from receiving ineffective treatment, making this not only a potential biomarker but also as a target for a new type of cancer treatment. "Predicting drug resistance is critical for precision oncology," said senior author Prof Virshup. "This work reveals how cancers can evade dependencies on Wnt signalling and serves as a solid foundation for further development." "We can now try to target those backup pathways activated by the FBXW7 mutation to overcome the drug resistance," added Dr Zhong, pointing to new treatment possibilities. The findings add to previous work by the scientists on how pancreatic cancers become resistant to treatment. Together, these discoveries increase our understanding of the ways cancers find alternate routes to grow and survive. With more precise therapeutic targets to lock onto, these findings bring the promise of personalised therapies one step closer to reality. In addition to the discovery of FBXW7, the team found these Wnt inhibitor-resistant tumours to be susceptible to an experimental drug known as dinaciclib. Their next step is to investigate the potential of dinaciclib alone and in combination with other agents in treating these cancers. "Our ultimate goal is to help patients with fully resistant tumours by targeting the alternate cancer pathways unleashed by FBXW7 mutations," said Prof Virshup. "We hope to translate our findings into more tailored and potent treatment strategies." "This research exemplifies the highly translational nature of the basic scientific research conducted at Duke-NUS. Cancers are notoriously diverse, and it is important that we can understand and map that diversity, so that we can offer truly personalised treatment that is effective for the individual and not leave patients to undergo unnecessary therapies that will not work for them," said Professor Patrick Tan, Senior Vice-Dean for Research at Duke-NUS. "This study is another important step on our journey to make every cancer a treatable disease and the team's exemplifies our resolve to deliver more effective therapies to patients." [1] Colorectal cancers are the second most common type of cancer diagnosed in Singapore for both men and women. Pancreatic cancer is the 10th most common cause of cancer in men in Singapore. The World Health Organisation estimated that in 2020 alone, more than 1.9 million new cases of colorectal cancers were diagnosed worldwide. [2] Duke-NUS, together with A*STAR, developed a made-in-Singapore Wnt inhibitor called ETC-159 which is currently in early phase clinical trials.

15 Sep 2023

·synapse.patsnap.com

CDK2 Inhibitor——Important Regulator of Cell Cycle Control

Cyclin-dependent kinases (CDKs), a serine/threonine family kinase, play a key role in cell cycle regulation and transcriptional activity. The activity of CDKs depends on their associated Cyclin subunits and non-catalytic regulatory proteins, which form CDK-Cyclin heterodimer complexes, playing a crucial role in regulating different biological processes. These processes include angiogenesis, hematopoiesis, gene transcription, apoptosis, neuronal activity, metabolism, DNA repair, exocytosis, and spermatogenesis. To date, at least nine types of CDKs have been identified in humans, labeled as CDK1-CDK9. In different tumor cells, cell cycle dysregulation often accompanies changes in CDK activity and/or its interacting proteins. Hence, the development of novel CDK inhibitors becomes an effective approach to combat various malignancies. CDK2, or cyclin-dependent kinase 2, is a crucial protein involved in cell cycle regulation in the human body. It plays a pivotal role in controlling the progression of cells from the G1 phase to the S phase, allowing DNA replication and cell division to occur. CDK2 forms complexes with cyclins, which activate its kinase activity, leading to the phosphorylation of various target proteins involved in cell cycle progression. Dysregulation of CDK2 activity has been implicated in numerous diseases, including cancer, making it an attractive target for therapeutic interventions aimed at controlling cell proliferation and promoting healthy cell cycle progression. CDK2 Competitive LandscapeAccording to the data provided by Patsnap Synapse-Global Drug Intelligence Database: the following figure shows that as of 10 Sep 2023, there are a total of 64 CDK2 drugs worldwide, from 72 organizations, covering 69 indications, and conducting 75 clinical trials. 👇Please click on the picture link below for free registration or login directly if you have freemium accounts, you can browse the latest research progress on drugs , indications, organizations, clinical trials, clinical results, and drug patents related to this target. The analysis of the target CDK2 reveals that Merck KGaA, Pfizer Inc., and Cyclacel Pharmaceuticals, Inc. are the companies with the highest stage of development. The drugs under the target CDK2 have been approved for indications such as B-Cell Chronic Lymphocytic Leukemia, Non-Small Cell Lung Cancer, Ovarian Cancer, and Triple Negative Breast Cancer. Small molecule drugs are progressing most rapidly, indicating intense competition in the market. The United States, European Union, and several other countries are actively developing drugs targeting CDK2. Overall, the target CDK2 shows a competitive landscape with potential for future development in various indications and drug types. The multi-target CDK2 inhibitor Dinaciclib enters phase III clinical trialsDinaciclib is a small molecule drug that targets multiple CDKs, including CDK1, CDK2, CDK5, and CDK9. It is being developed by Merck & Co., Inc. and is currently in Phase 3, which is the final stage of clinical trials before seeking regulatory approval. The drug has shown potential therapeutic benefits in the treatment of neoplasms, immune system diseases, and hemic and lymphatic diseases. Specifically, it has demonstrated efficacy in B-cell chronic lymphocytic leukemia (B-CLL) and acute myeloid leukemia (AML). These indications are characterized by the abnormal growth and proliferation of certain cells in the blood and bone marrow. 👇Please click on the image below to directly access the latest data (R&D Status | Core Patent | Clinical Trial | Approval status in Global countries) of this drug. Dinaciclib's mechanism of action involves inhibiting CDKs, which are enzymes involved in cell cycle regulation and transcriptional control. By targeting multiple CDKs, the drug aims to disrupt the abnormal cell growth and division observed in cancer and other diseases. One notable aspect of Dinaciclib is its orphan drug status. Orphan drugs are medications developed to treat rare diseases or conditions that affect a small number of patients. This designation provides certain incentives and benefits to the drug developer, such as extended market exclusivity and financial support for clinical trials. Overall, Dinaciclib holds promise as a potential treatment option for B-CLL and AML, two types of leukemia. Its small molecule nature and ability to target multiple CDKs make it an interesting candidate for further development. The ongoing Phase 3 trials will provide crucial data on its safety and efficacy, which will determine its potential for regulatory approval and commercialization. Selective CDK2 inhibitor PF-07104091 enters Phase II clinical trialThe drug PF-07104091 is a small molecule drug that targets CDK2, a protein involved in cell cycle regulation. It is being developed by Pfizer Inc., a leading pharmaceutical company. PF-07104091 has shown potential in treating various therapeutic areas, including neoplasms (abnormal growth of cells), skin and musculoskeletal diseases, endocrinology and metabolic diseases, respiratory diseases, and urogenital diseases. It is specifically indicated for non-small cell lung cancer, ovarian cancer, small cell lung cancer, triple negative breast cancer, solid tumors, breast cancer, and hormone receptor positive HER2 negative breast cancer. 👇Please click on the image below to directly access the latest data (R&D Status | Core Patent | Clinical Trial | Approval status in Global countries) of this drug. Currently, PF-07104091 has reached Phase 2 of clinical development globally. In China, it has reached Phase 1/2, indicating that it is still in the early stages of development in this region. The objective presentation of this information allows stakeholders in the pharmaceutical industry to understand the key details of PF-07104091. The drug's small molecule nature suggests that it may have advantages in terms of formulation and delivery. Its target, CDK2, is a well-known protein involved in cell cycle regulation, making it a promising target for therapeutic intervention. The wide range of therapeutic areas and indications for PF-07104091 indicates its potential for treating various diseases. Non-small cell lung cancer, ovarian cancer, and breast cancer are among the most prevalent and challenging cancers globally, making the drug's potential impact significant. The fact that PF-07104091 has reached Phase 2 globally suggests that it has shown promising results in early clinical trials, demonstrating its safety and efficacy to a certain extent. However, its current phase in China, Phase 1/2, indicates that further research and development are needed to establish its effectiveness in this specific market. In summary, PF-07104091 is a small molecule drug developed by Pfizer Inc. that targets CDK2. It has shown potential in treating various therapeutic areas and indications, particularly in the field of oncology. While it has reached Phase 2 globally, further development is required in China. This objective summary provides a concise overview of the drug's key details, allowing stakeholders to assess its potential and make informed decisions.

100 Deals associated with Dinaciclib

External Link

KEGG	Wiki	ATC	Drug Bank
D09604	Dinaciclib	-	DB12021

R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Chronic lymphocytic leukaemia refractory	Phase 3	-	Merck Sharp & Dohme Corp.	01 Aug 2012
Mantle cell lymphoma refractory	Phase 2	-	Merck Sharp & Dohme Corp.	01 Mar 2009
Acute Lymphoblastic Leukemia	Phase 2	-	Merck Sharp & Dohme Corp.	01 Jan 2009
Acute Myeloid Leukemia	Phase 2	-	Merck Sharp & Dohme Corp.	01 Jan 2009
Breast Cancer	Phase 2	-	Merck Sharp & Dohme Corp.	01 Jul 2008
Non-Small Cell Lung Cancer	Phase 2	-	Merck Sharp & Dohme Corp.	01 Jul 2008
Relapsing acute myeloid leukemia	Phase 1	United States	AbbVie, Inc.	23 Jul 2018
Relapsing acute myeloid leukemia	Phase 1	Australia	AbbVie, Inc.	23 Jul 2018
Relapsing acute myeloid leukemia	Phase 1	Spain	AbbVie, Inc.	23 Jul 2018
Advanced breast cancer	Phase 1	United States	Merck Sharp & Dohme Corp.	28 Dec 2016

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT00937937 (Pubmed \| Cancer) Manual	Phase 2	Melanoma	72	SCH 727965 50 mg/m2	pyxppgyehc(izjgejsmne) = indrtuyxcp naxejfquzr (qpwjygexxa, 5.5 - 10.5) View more	Negative	29 Sep 2024
NCT02684617 (KEYNOTE-155, CTgov)	Phase 1	Multiple Myeloma	75	dinaciclib+pembrolizumab (rrCLL Cohort)	jtmrshfiab = uycgahdhxa albtdjjtkt (zygsvfodbt, tcesdrizqc - hdhsmfpxsg) View more	-	01 Mar 2021
NCT02684617 (KEYNOTE-155, CTgov)	Phase 1	Multiple Myeloma	75	dinaciclib+pembrolizumab (rrMM Cohort)	jtmrshfiab = wdolegvxar albtdjjtkt (zygsvfodbt, cuxxkzoyra - loqrvosltt) View more	-	01 Mar 2021
NCT01783171 (Pubmed \| Clin Transl Sci) Manual	Phase 1	Pancreatic Cancer	39	MK-2206+Dinaciclib	jizgpvsmcn(vrgtcsgpea) = dinaciclib 9 mg/m2 and MK-2206 135 mg btahhjuqxb (hffexpcqkx ) View more	Negative	01 Nov 2020
NCT01676753 (ASCO 12020 \| ASCO 22020) Manual	Phase 1	Triple Negative Breast Cancer HER2 Negative \| ER Negative \| PR Negative	32	dinaciclib+pembrolizumab	zrckhpkmna(jztyqjdxxr) = The RP2D of dina given in combination with standard dose P is 33 mg/m2 hfesdvvelc (higbhzcjbj ) View more	Positive	29 May 2020
NCT01676753 (ASCO2019)	Phase 1	Triple Negative Breast Cancer	22	Dinaciclib + Pembrolizumab	mtpynjfohb(judfrrwzre) = awvofvqaox lzxdklfkyz (fpeikzbane ) View more	-	26 May 2019
NCT01515176 (CTgov)	Phase 1/2	Chronic lymphocytic leukaemia refractory \| B-Cell Prolymphocytic Leukemia \| Small Lymphocytic Lymphoma	36	Pharmacological Study+Dinaciclib+Ofatumumab	vdmoogatej = pqdbjpqzua bgkoyfuenx (caemhzoskq, ikizjpkctd - qxmscbfdtr) View more	-	15 Mar 2018
NCT00871910 (P04630, Pubmed \| Med J Aust \| Br J Cancer) Manual	Phase 1	Neoplasms	61	dinaciclib	tqeszdhtuo(dpxmnyvdmr) = pancytopenia, neutropenic fever, elevated transaminases, hyperuricemia and hypotension fjercgrmrc (tapyrksstw ) View more	Positive	24 Oct 2017
AACR2017	Phase 1	HR-positive/HER2-low Solid Tumors	-	Dinaciclib + Veliparib	zvkkqyuany(acwbflbysl) = vlmufttieg glfoyemlam (pbepzsuffl )	-	01 Jul 2017
NCT01624441 (Pubmed \| Invest New Drugs) Manual	Phase 1	Triple Negative Breast Cancer triple negative	9	dinaciclib +epirubicin	epfwxfwciz(vejkwhtopx) = neutropenia (grade 3, n = 2), syncope (grade 3, n = 2) and vomiting (grade 3, n = 1) rjiebnomkx (cejtymylrx )	Negative	01 Aug 2015
NCT00871663 (P04629, Pubmed \| Leukemia) Manual	Phase 1	Chronic Lymphocytic Leukemia	52	Dinaciclib	koahoytahc(lceazstiwd) = cytopenias, transient laboratory abnormalities and TLS xthjevskfs (zffxjtphqu )	Positive	01 Jul 2015
NCT00871663 (P04629, Pubmed \| Leukemia) Manual	Phase 1	Chronic Lymphocytic Leukemia	52	Dinaciclib (14 mg/m2)		Positive	01 Jul 2015

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