Search company, investor...

Predict your next investment

Amgen company logo
Corporation
HEALTHCARE | Biotechnology
amgen.com

Investments

11

Portfolio Exits

10

Partners & Customers

10

Service Providers

1

About Amgen

Amgen (NASDAQ: AMGN) is a biotechnology company. It focuses on areas of high unmet medical need and leverages its biologics manufacturing expertise to strive for solutions that improve health outcomes and people's lives. Amgen was formerly known as Applied Molecular Genetics. The company was founded in 1980 and is based in Thousand Oaks, California.

Headquarters Location

One Amgen Center Drive

Thousand Oaks, California, 91320,

United States

805-447-1000

Are you an investor?
Submit your portfolio details now to be considered in our investor rankings.

Research containing Amgen

Get data-driven expert analysis from the CB Insights Intelligence Unit.

CB Insights Intelligence Analysts have mentioned Amgen in 2 CB Insights research briefs, most recently on Jan 5, 2024.

Latest Amgen News

A genome-wide CRISPR screen identifies BRD4 as a regulator of cardiomyocyte differentiation

Feb 23, 2024

Abstract Human induced pluripotent stem cell (hiPSC) to cardiomyocyte (CM) differentiation has reshaped approaches to studying cardiac development and disease. In this study, we employed a genome-wide CRISPR screen in a hiPSC to CM differentiation system and reveal here that BRD4, a member of the bromodomain and extraterminal (BET) family, regulates CM differentiation. Chemical inhibition of BET proteins in mouse embryonic stem cell (mESC)-derived or hiPSC-derived cardiac progenitor cells (CPCs) results in decreased CM differentiation and persistence of cells expressing progenitor markers. In vivo, BRD4 deletion in second heart field (SHF) CPCs results in embryonic or early postnatal lethality, with mutants demonstrating myocardial hypoplasia and an increase in CPCs. Single-cell transcriptomics identified a subpopulation of SHF CPCs that is sensitive to BRD4 loss and associated with attenuated CM lineage-specific gene programs. These results highlight a previously unrecognized role for BRD4 in CM fate determination during development and a heterogenous requirement for BRD4 among SHF CPCs. Access options $119.00 per year Prices vary by article type from$1.95 Additional access options: Fig. 2: Brd4 deletion in ISL1+ progenitors in vivo results in myocardial hypoplasia. Fig. 3: Brd4 deletion in SHF progenitors in vivo recapitulates loss in ISL1+ progenitors. Fig. 4: Loss of BRD4 in vivo attenuates cardiac differentiation-related gene expression. Fig. 5: BRD4 is enriched at transcriptionally active regions of chromatin marked by H3K4Me3. Fig. 6: BRD4 specifically regulates an MSX1/2+ progenitor population. Data availability All data supporting the findings of this study are included in the main article and associated files, and Source Data have been provided with this manuscript. All transcriptomic and epigenomic data are available in the Gene Expression Omnibus database under accession number GSE184922 , which is available at https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE184922 . References Van Der Linde, D. et al. Birth prevalence of congenital heart disease worldwide: a systematic review and meta-analysis. J. Am. Coll. Cardiol. 58, 2241–2247 (2011). Filippakopoulos, P. et al. Selective inhibition of BET bromodomains. Nature 468, 1067–1073 (2010). Nomaru, H. et al. Single cell multi-omic analysis identifies a Tbx1-dependent multilineage primed population in the murine cardiopharyngeal mesoderm. Nat. Commun. 12, 6645 (2021). Chen, Y.-H., Ishii, M., Sun, J., Sucov, H. M. & Maxson, R. E. Jr. Msx1 and Msx2 regulate survival of secondary heart field precursors and post-migratory proliferation of cardiac neural crest in the outflow tract. Dev. Biol. 308, 421–437 (2007). Dawson, M. A. The cancer epigenome: concepts, challenges, and therapeutic opportunities. Science 355, 1147–1152 (2017). Nagy A., Gertsenstein, M., Vintersten, K. & Behringer, R. (eds) Manipulating the Mouse Embryo: A Laboratory Manual 3rd edn (Cold Spring Harbor Laboratory Press, 2003). Poleshko, A. et al. Genome-nuclear lamina interactions regulate cardiac stem cell lineage restriction. Cell 171, 573–587 (2017). Kattman, S. J. et al. Stage-specific optimization of activin/nodal and BMP signaling promotes cardiac differentiation of mouse and human pluripotent stem cell lines. Cell Stem Cell 8, 228–240 (2011). Shah, P. P. et al. Pathogenic LMNA variants disrupt cardiac lamina-chromatin interactions and de-repress alternative fate genes. Cell Stem Cell 28, 938–954 (2021). Robinson, M. D., McCarthy, D. J. & Smyth, G. K. edgeR: a Bioconductor package for differential expression analysis of digital gene expression data. Bioinformatics 26, 139–140 (2010). Robinson, M., McCarthy, D. J., Chen, Y. & Smyth, G. K. Package ‘edger’. Preprint at http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.367.3149&rep=rep1&type=pdf (2012). Stuart, T. et al. Comprehensive integration of single-cell data. Cell 177, 1888–1902 (2019). Cheshire, C. et al. nf-core/cutandrun: nf-core/cutandrun v3.2 Tin Albatross. https://doi.org/10.5281/zenodo.8305872 (2023). Acknowledgements The authors thank the Srivastava and Jain laboratories for critical discussions and feedback and K. Ozato (National Institutes of Health) for experimental reagents. We are grateful to V. Vedantham (University of California, San Francisco (UCSF)), S. Hota (Gladstone Institutes), I. Kathiriya (UCSF) and M. Costa (Gladstone Institutes) for thoughtful commentary on the manuscript. We thank B. Taylor (Gladstone Institutes) and K. Claiborn (Gladstone Institutes) for editorial assistance as well as A. Silva (Ana Silva Illustrations) and G. Maki (Gladstone Institutes) for assistance with illustrations. We thank the University of Pennsylvania iPSC core for technical assistance. This work was supported by the NIH (R35 HL166663 and R01 HL139783; F31 HL147416 to R.L-S.; K08HL157700 to A.P. ; P01 HL146366, R01 HL057181, R01 HL127240 and R01 HL015100 to D.S. ), the Burroughs Wellcome Foundation Career Award for Medical Scientists (R.J.), the Allen Foundation (R.J.), the American Heart Association (R.J. and S.M. ), the National Science Foundation (15-48571 to R.J.), the Swiss National Science Foundation (P400PM_186704 and P2LAP3_178056 to M.A. ), the Japan Society for the Promotion of Science Overseas Research Fellowship (T.N. ), the Sarnoff Cardiovascular Research Foundation (A.P. ), the Michael Antonov Charitable Foundation (A.P. ), the Frank A. Campini Foundation (A.P. ), the Tobacco‐Related Disease Research Program (578649 to A.P. ), the A. P. Giannini Foundation (P0527061 to A.P. ), the Roddenberry Foundation (D.S. ), the L. K. Whittier Foundation (D.S. ), Dario and Irina Sattui (D.S.) and the Younger Family Fund (D.S.). Author information Authors and Affiliations Gladstone Institutes, San Francisco, CA, USA Arun Padmanabhan, T. Yvanka de Soysa, Angelo Pelonero, Clara Youngna Lee, Nandhini Sadagopan, Tomohiro Nishino, Lin Ye, Sanjeev S. Ranade, Michael Alexanian, Saptarsi M. Haldar & Deepak Srivastava Department of Medicine, University of California, San Francisco, School of Medicine, San Francisco, CA, USA Arun Padmanabhan, Clara Youngna Lee, Nandhini Sadagopan & Saptarsi M. Haldar Chan Zuckerberg Biohub, San Francisco, CA, USA Arun Padmanabhan Valerie Sapp & Mohit Jain Valerie Sapp & Mohit Jain Cardiovascular Institute, Epigenetics Institute, and Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA Parisha P. Shah, Qiaohong Wang, Li Li, Rachel Yang, Ashley Karnay, Nikhita Bolar, Ricardo Linares-Saldana & Rajan Jain Department of Cell and Developmental Biology, University of Pennsylvania, Philadelphia, PA, USA Parisha P. Shah, Qiaohong Wang, Li Li, Rachel Yang, Ashley Karnay, Andrey Poleshko, Nikhita Bolar, Ricardo Linares-Saldana & Rajan Jain Department of Pediatrics, University of California, San Francisco, School of Medicine, San Francisco, CA, USA Michael Alexanian & Deepak Srivastava Sarah U. Morton Sarah U. Morton Deepak Srivastava Deepak Srivastava T. Yvanka de Soysa Angelo Pelonero Valerie Sapp Parisha P. Shah Qiaohong Wang Li Li Clara Youngna Lee Nandhini Sadagopan Tomohiro Nishino Lin Ye Rachel Yang Ashley Karnay Andrey Poleshko Nikhita Bolar Ricardo Linares-Saldana Sanjeev S. Ranade Michael Alexanian Sarah U. Morton Mohit Jain Saptarsi M. Haldar Deepak Srivastava Rajan Jain Contributions A.P., R.J. and D.S. conceived and designed the study. A.P., Y.d.S., V.S., P.P.S., Q.W., L.L., C.Y.L., N.S., A. Poleshko, N.B., R.L.-S., T.N. and L.Y. performed all the experiments. A.P., Y.d.S., V.S., A. Pelonero, S.U.M., M.J., R.Y., A.K., L.Y. and R.J. analyzed the data. M.A., S.M.H. and D.S. assisted with data interpretation. A.P. and R.J. wrote the manuscript. D.S. and R.J. supervised the project. All authors edited and approved the manuscript. Corresponding authors Competing interests D.S. is a scientific co-founder, shareholder and director of Tenaya Therapeutics. S.M.H. is an executive, officer and shareholder of Amgen and is a scientific co-founder and shareholder of Tenaya Therapeutics. M.J. is founder, shareholder and executive of Sapient Bioanalytics, LLC. The remaining authors declare no competing interests. Peer review Peer review information Nature Cardiovascular Research thanks Bernice Morrow, John Hinson, Michael A. Burke, Lijie Shi and the other, anonymous, reviewer(s) for their contribution to the peer review of this work. Additional information Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Extended data (a) Top 1000 genes ranked by enrichment or depletion. (b, c) Categorization of top 200 genes enriched (b) or depleted (c) in cardiac myocytes compared to undifferentiated hiPSCs by biological groups. (d, e) Gene ontology (GO) analysis of top enriched (d) or depleted (e) hits (see Methods for details). (f-g) Venn diagrams demonstrating the number of CHD (f) or Non-CHD (g) probands with predicted damaging DNVs in hits identified in our screen as enriching hiPSC:CM differentiation or depleting hiPSC:CM differentiation. Arrows depict Venn diagrams representing the number of probands from each cohort with predicted damaging DNVs identified in our screen that have mutations in known dominant CHD genes or where these candidate CHD genes may potentially be causative. (h) Venn diagram demonstrating the number of CHD probands with (purple) or without (brown) damaging DNVs in hits identified in our screen highlighting no enrichment for extracardiac anomalies (p = 0.43) or neurodevelopmental delay (NDD; p = 0.23) and a slight enrichment for conotruncal CHD (p = 0.04). (i) TNNT2+ cells quantified by flow cytometry at day 10 of hiPSC to CM differentiation in WTC11 cells treated with 100 nM JQ1 starting at day 6 (n = 3 biologically independent samples). (j) MZ3 treatment (500 nM for 0, 3.5, 7, and 16 hours) effectively degrades BRD4 in SV20 hiPSCs as assessed by immunoblot analysis for BRD4 with β-actin expression as a loading control. In all graphs, error bars represent ±1 SEM. * represents p = 0.0271 (two-tailed unpaired t test). (a) Expression of Myh6, Nkx2-5, and Tnnt2 at day 7 of mESCs cardiac differentiation treated with JQ1 (100 nM) starting day 5 of differentiation (n = 3 biologically independent samples). (b) TNNT2+ cells quantified by flow cytometry at d9 of mESC differentiation in CMV-CreERT2;Brd4flox/flox cells treated with 4-hydroxytamoxifen (TAM), JQ1 (250 nM) or MZ3 (500 nM) starting at day 5 (n = 3 biologically independent samples; FACS gating strategy in Supplementary Fig. 1 ). (c-d) Immunofluorescence of TNNT2 at day 9 of mESC to CM differentiation in wild type cells treated with JQ1 (100 nM) or vehicle starting at day 5. (e-f) Immunofluorescence of BRD4 in vehicle (ethanol, e-e′′) and TAM (f-f′′) treated undifferentiated mESCs. (g) Volcano plot showing RNA-seq from CMV-CreERT2;Brd4flox/flox (TAM vs. vehicle [VEH]) mESCs and gene ontology analysis of downregulated and upregulated genes (see Methods for details). (h) Heatmap showing expression of select transcription factor and muscle structural protein genes from RNA-seq in CMV-CreERT2;Brd4flox/flox (TAM vs. VEH) mESC-derived cardiac tissues (day 10; TAM or VEH added at day 5). In all graphs, error bars represent ±1 SEM. For a, all comparisons are made relative to 0 nM compound for each gene; * represents p < 0.0493, ** represents p < 0.0085 (two-tailed unpaired t test). For b, all comparisons are made relative to VEH for each condition; * represents p < 0.0188 (two-tailed unpaired t test). Scale Bars = 100 µm (c, d, e, e′, e′′, f, f′, f′′). (a) Lineage tracing of Isl1Cre/+;Brd4flox/+ and Isl1Cre/+;Brd4flox/flox with R26mTmG/+ allele. Immunohistochemistry of ISL1-derived cells (GFP) and TNNT2 or BRD4 (red) in heart and quantitative assessment of right ventricular myocardial wall thickness in indicated genotypes at E14 (5 sections from n = 2 control embryos and 11 sections from n = 4 mutant embryos). (b) Hematoxylin and eosin staining of a section through outflow tract and RV of Isl1Cre/+;Brd4flox/+ and Isl1Cre/+;Brd4flox/flox embryos at E12.5 and quantitative assessment of right ventricular myocardial wall thickness in indicated genotypes (10 sections from n = 2 control embryos and 11 sections from n = 2 mutant embryos). (c) Quantification of percentage phospho-histone H3-, cleaved caspase 3-, and TUNEL-positive cells in the RV of E12.5 and E14.5 embryos of indicated genotypes (n = 2 biologically independent samples per genotype at E12.5; n = 3-4 biologically independent samples per genotype at E14.5). (d) Hematoxylin and eosin staining of a section through outflow tract and RV of Isl1Cre/+;Brd4flox/+ and Isl1Cre/+;Brd4flox/flox embryos at E10 and quantitative assessment of right ventricular myocardial wall thickness in indicated genotypes (9 sections from n = 3 control embryos and 8 sections from n = 3 mutant embryos). (e) Quantification of percentage phospho-histone H3- and TUNEL-positive cells in the RV of E10 control (Isl1Cre/+;Brd4flox/+ or Brd4flox/flox) and Isl1Cre/+;Brd4flox/flox embryos (n = 4 biologically independent samples per condition). (f) BRD4 and TNNT2 immunohistochemistry along with lineage tracing with R26mTmG/+ allele in Isl1Cre/+;Brd4flox/+ and Isl1Cre/+;Brd4flox/flox E9.5 embryos at level of right ventricle. Error bars represent ±1 SEM. All comparisons are made as indicated; * represents p = 0.0091, ** represents p = 0.0021, **** represents p < 0.0001 (two-tailed unpaired t test). RV, right ventricle; LV, left ventricle; OT, outflow tract. Scale Bars = 100 µm (a, b, d, f). (a) Hematoxylin and eosin staining of a section through outflow tract and RV of Mef2c-AHF-Cre;Brd4flox/+ and Mef2c-AHF-Cre;Brd4flox/flox embryos at E13.5 and quantitative assessment of right ventricular myocardial wall thickness in indicated genotypes (19 sections from n = 3 control embryos and 18 sections from n = 3 mutant embryos). (b) Quantification of percentage phospho-histone H3- and cleaved caspase 3-positive cells in the RV of E13.5 Mef2c-AHF-Cre;Brd4flox/+ and Mef2c-AHF-Cre;Brd4flox/flox embryos (n = 3-4 biologically independent samples per genotype). (c) Hematoxylin and eosin staining of a section through outflow tract and RV of Mef2c-AHF-Cre;Brd4flox/+ and Mef2c-AHF-Cre;Brd4flox/flox embryos at E10.5 and quantitative assessment of right ventricular myocardial wall thickness in indicated genotypes (6 sections from n = 3 control embryos and 6 sections from n = 3 mutant embryos). (d) Quantification of percentage phospho-histone H3- and cleaved caspase 3-positive cells in the RV of E10.5 Mef2c-AHF-Cre;Brd4flox/+ and Mef2c-AHF-Cre;Brd4flox/flox embryos (n = 3 biologically independent samples per genotype). Error bars represent ±1 SEM. All comparisons are made as indicated; * represents p = 0.0489, ** represents p = 0.0146, **** represents p < 0.0001 (two-tailed unpaired t test). RV, right ventricle; LV, left ventricle. Scale Bars = 100 µm (a, c). (a) Image of Brd4flox/flox embryo appearing in Fig. 2i with region microdissected for bulk RNA-seq highlighted in red. (b) Principal component analysis of RNA-seq from Isl1Cre/+;Brd4flox/+ (blue) and Isl1Cre/+;Brd4flox/flox (red) E9.5 embryos. (c) Volcano plots of E9.5 Isl1Cre/+;Brd4flox/+ vs. Isl1Cre/+;Brd4flox/flox embryonic hearts (same data appearing in Fig. 4 ) with a subset of cardiac and Wnt-related genes annotated (see Methods for details). Brd4flox/flox(d, f) and Isl1Cre/+;Brd4flox/flox (e, g) E9.5 embryos at level of right ventricle stained with ISL1 (red, d-e), BRD4 (green, d-e), or AXIN2 (green, f-g). Note the expansion of ISL1- (arrow heads) and AXIN2- (dotted line) expressing cells into the RV from distal outflow tract in mutant embryos. (h-m) ISL1 and AXIN2 Immunohistochemistry of E10.5 Mef2c-AHF-Cre;Brd4flox/+ (h,k) and Mef2c-AHF-Cre;Brd4flox/flox (i,j,l,m) embryos at the level of outflow tract. (h-j, ISL1; k-m, AXIN2). Note the expansion of ISL1- (arrow heads) and AXIN2- (dotted line) expressing cells into the right ventricle from distal outflow tract in mutant embryos. (n-o) AXIN2 RNAscope of Brd4flox/flox (n,n′) and Isl1Cre/+;Brd4flox/flox (o,o′) E9.5 embryos at the level of the right ventricle (n′ and o′ are magnified images of n and o, respectively). (p-q) ISL1 representative immunofluorescence at day 8 of mESC-derived cardiac cultures treated with vehicle (DMSO; VEH) (p) or JQ1 (500 nM) (q) starting at day 5. (r) Isl1 expression in day 8-9 mESC-derived cardiac cultures treated with increasing doses of JQ1 (0–500 nM; JQ1 added at day 5; n = 3 n = 3 biologically independent samples per dose). (s-t) AXIN2 RNAscope of Mef2c-AHF-Cre;Brd4flox/+ (s,s′) and Mef2c-AHF-Cre;Brd4flox/flox (t,t′) E10.5 embryos at level of right ventricle (s′ and t′ are magnified images of s and t, respectively). For r, all comparisons are made relative to 0 nM compound. *** represents p = 0.0007 (two-tailed unpaired t test). RV, right ventricle; OT, outflow tract. Scale Bar = 250 µm (a), 50 µm (d-m, n, o, s, t), 100 µm (p, q, n′, o′, s′, t′). (a) Attenuating Wnt signaling at the CPC stage (day 5) in mESC to CM differentiation by doubling the normal concentration of the small molecule Wnt inhibitor XAV939 concomitant with Brd4 genetic deletion by 4-hydroxytamoxifen treatment (TAM) in CMV-CreERT2;Brd4flox/flox mESCs partially normalizes expression of CPC markers and Msx1/2 by qRT-PCR (n = 3-4 biologically independent samples per genotype). (b-e) Attenuating Wnt signaling at the CPC stage (day 5) in mESC to CM differentiation by doubling the normal concentration of the small molecule Wnt inhibitor XAV939 concomitant with Brd4 genetic deletion by 4-hydroxytamoxifen treatment (TAM) in CMV-CreERT2;Brd4flox/flox mESCs partially normalizes TNNT2 staining by immunofluorescence at day 9 of CM differentiation (for e, n = 3 biologically independent samples per condition). (f, g) Attenuation of Wnt signaling at the CPC stage (day 6) in hiPSC to CM differentiation by addition of the small molecule Wnt inhibitor IWP4 (5 μM for low dose and 10 μM high dose) concomitant with BET inhibition using JQ1 (25 nM for low dose and 50 nM for high dose) increases the number of TNNT2+ cells as assessed by flow cytometry (n = 3 biologically independent samples per condition; gating strategy in Supplementary Fig. 2 ). Error bars represent ±1 SEM. For a,e,f,g all comparisons are made with p values as indicated (two-way ANOVA with Tukey’s multiple comparisons test). (a-c) UMAP plots of all cells (n = 23,592) collected from the microdissected heart and surrounding pharyngeal mesoderm (n = 2 embryos per genotype) (a), labeled by sample identity (b), and number of features (c). (d) Feature plots for expression of example marker genes used to define cell types (for example, Hbb-y for blood cells; Dlx2, Dlx5, and Twist1 for neural crest cells; Lhx2 and Foxc2 for branchiomeric muscle progenitors; Epcam for endoderm). (e-g) UMAP plots demonstrate expression of the Cre transgene (e) occurs in clusters marked by high Mef2c (f) and Isl1 (g) expression, consistent with Cre driven in Mef2c-expressing second heart field cells. (h) Clusters of Cre expressing cells detected at E9.5 in our scRNA-seq dataset selected for further analysis (n = 4,640). (i) Feature plot for Cre expression in a UMAP of cells from (h) following normalization and reclustering. (h’-i’) Cluster 0 cells highlighted in red on UMAP plots from h and i.

Amgen Investments

11 Investments

Amgen has made 11 investments. Their latest investment was in Quantinuum as part of their Series A on January 04, 2024.

CBI Logo

Amgen Investments Activity

investments chart

Date

Round

Company

Amount

New?

Co-Investors

Sources

1/4/2024

Series A

Quantinuum

$300M

Yes

7

9/14/2023

Series C

Generate Biomedicines

$273M

Yes

4

10/11/2022

Series B

Neumora

$112M

No

11

10/7/2021

Series A

Subscribe to see more

$99M

Subscribe to see more

10

11/13/2020

Grant - III

Subscribe to see more

$99M

Subscribe to see more

10

Date

1/4/2024

9/14/2023

10/11/2022

10/7/2021

11/13/2020

Round

Series A

Series C

Series B

Series A

Grant - III

Company

Quantinuum

Generate Biomedicines

Neumora

Subscribe to see more

Subscribe to see more

Amount

$300M

$273M

$112M

$99M

$99M

New?

Yes

Yes

No

Subscribe to see more

Subscribe to see more

Co-Investors

Sources

7

4

11

10

10

Amgen Portfolio Exits

10 Portfolio Exits

Amgen has 10 portfolio exits. Their latest portfolio exit was Neumora on September 15, 2023.

Date

Exit

Companies

Valuation
Valuations are submitted by companies, mined from state filings or news, provided by VentureSource, or based on a comparables valuation model.

Acquirer

Sources

9/15/2023

IPO

$99M

Public

4

6/29/2022

Acquired - II

$99M

1

11/30/2021

IPO - II

$99M

Public

24

9/30/2021

IPO

Subscribe to see more

$99M

Subscribe to see more

10

7/2/2020

Reverse Merger

Subscribe to see more

$99M

Subscribe to see more

10

Date

9/15/2023

6/29/2022

11/30/2021

9/30/2021

7/2/2020

Exit

IPO

Acquired - II

IPO - II

IPO

Reverse Merger

Companies

Subscribe to see more

Subscribe to see more

Valuation

$99M

$99M

$99M

$99M

$99M

Acquirer

Public

Public

Subscribe to see more

Subscribe to see more

Sources

4

1

24

10

10

Amgen Acquisitions

26 Acquisitions

Amgen acquired 26 companies. Their latest acquisition was Horizon Therapeutics on October 06, 2023.

Date

Investment Stage

Companies

Valuation
Valuations are submitted by companies, mined from state filings or news, provided by VentureSource, or based on a comparables valuation model.

Total Funding

Note

Sources

10/6/2023

Debt

$99M

$98M

Acq - P2P

7

10/20/2022

Series D

$99M

$139.14M

Acq - P2P

3

7/27/2021

$99M

Acquired

10

4/16/2021

Other

Subscribe to see more

$99M

$99M

Subscribe to see more

10

3/30/2021

Series B

Subscribe to see more

$99M

$99M

Subscribe to see more

10

Date

10/6/2023

10/20/2022

7/27/2021

4/16/2021

3/30/2021

Investment Stage

Debt

Series D

Other

Series B

Companies

Subscribe to see more

Subscribe to see more

Valuation

$99M

$99M

$99M

$99M

$99M

Total Funding

$98M

$139.14M

$99M

$99M

Note

Acq - P2P

Acq - P2P

Acquired

Subscribe to see more

Subscribe to see more

Sources

7

3

10

10

10

Amgen Partners & Customers

10 Partners and customers

Amgen has 10 strategic partners and customers. Amgen recently partnered with Xeris Pharmaceuticals on January 1, 2024.

Date

Type

Business Partner

Country

News Snippet

Sources

1/10/2024

Licensor

United States

Xeris Biopharma Shares Climb 12% on Amgen License Agreement

Shares of Xeris Biopharma rose Wednesday after the company reached a license agreement with Amgen involving its XeriJect technology .

3

1/6/2024

Licensor

United States

Amgen Opts-in on Generate:Biomedicines Collaboration for Drug Development

With somewhere over $ 400 million in runway cash and Amgen 's decision to opt-in to the collaboration with Generate : Biomedicines , it 's possible that in a few years , we 'll experience the kinds of waves that the surfers in The Endless Summer dreamed of .

1

12/27/2023

Licensor

South Korea

LegoChem signs antibody deal with Amgen worth up to $1.25B

Amgen has entered into a collaboration and licensing agreement worth up to $ 1.25 B with South Korea 's LegoChem Biosciences for the development of antibody drug conjugates , or ADCs .

1

11/30/2023

Partner

United States

Subscribe to see more

Subscribe to see more

10

11/28/2023

Vendor

United States

Subscribe to see more

Subscribe to see more

10

Date

1/10/2024

1/6/2024

12/27/2023

11/30/2023

11/28/2023

Type

Licensor

Licensor

Licensor

Partner

Vendor

Business Partner

Country

United States

United States

South Korea

United States

United States

News Snippet

Xeris Biopharma Shares Climb 12% on Amgen License Agreement

Shares of Xeris Biopharma rose Wednesday after the company reached a license agreement with Amgen involving its XeriJect technology .

Amgen Opts-in on Generate:Biomedicines Collaboration for Drug Development

With somewhere over $ 400 million in runway cash and Amgen 's decision to opt-in to the collaboration with Generate : Biomedicines , it 's possible that in a few years , we 'll experience the kinds of waves that the surfers in The Endless Summer dreamed of .

LegoChem signs antibody deal with Amgen worth up to $1.25B

Amgen has entered into a collaboration and licensing agreement worth up to $ 1.25 B with South Korea 's LegoChem Biosciences for the development of antibody drug conjugates , or ADCs .

Subscribe to see more

Subscribe to see more

Subscribe to see more

Subscribe to see more

Sources

3

1

1

10

10

Amgen Service Providers

1 Service Provider

Amgen has 1 service provider relationship

Service Provider

Associated Rounds

Provider Type

Service Type

Acquired

Counsel

General Counsel

Service Provider

Associated Rounds

Acquired

Provider Type

Counsel

Service Type

General Counsel

Partnership data by VentureSource

Amgen Team

49 Team Members

Amgen has 49 team members, including current Chief Executive Officer, Robert A. Bradway.

Name

Work History

Title

Status

Robert A. Bradway

Chief Executive Officer

Current

Subscribe to see more

Subscribe to see more

Subscribe to see more

Subscribe to see more

Subscribe to see more

Subscribe to see more

Subscribe to see more

Subscribe to see more

Subscribe to see more

Subscribe to see more

Subscribe to see more

Subscribe to see more

Name

Robert A. Bradway

Subscribe to see more

Subscribe to see more

Subscribe to see more

Subscribe to see more

Work History

Title

Chief Executive Officer

Subscribe to see more

Subscribe to see more

Subscribe to see more

Subscribe to see more

Status

Current

Subscribe to see more

Subscribe to see more

Subscribe to see more

Subscribe to see more

Compare Amgen to Competitors

B
Boehringer Ingelheim

Boehringer Ingelheim operates as a biopharmaceutical company. The company's main offerings include therapies in areas of high unmet medical need, spanning three business areas such as human pharma, animal health, and biopharmaceutical contract manufacturing. It primarily serves the pharmaceutical and healthcare industries. The company was founded in 1885 and is based in Ingelheim am Rhein, Germany.

Sumitovant Logo
Sumitovant

Sumitovant is a technology-driven biopharmaceutical company that focuses on the development and commercialization of novel therapies. The company's main offerings include the development of treatments for patients with rare conditions and other diseases, utilizing their proprietary computing and data platforms and scientific expertise. These treatments address unmet needs in various areas such as pediatrics, urology, oncology, women's health, specialty respiratory, and infectious diseases. It was founded in 2019 and is based in New York, New York. Sumitovant operates as a subsidiary of Sumitomo Dainippon Pharma.

Ferring Pharmaceuticals Logo
Ferring Pharmaceuticals

Ferring Pharmaceuticals is a research-driven, specialty biopharmaceutical group. Ferring Pharmaceuticals specializes in the areas of reproductive medicine and women’s health, urology and gastroenterology.

I
Immunwork

Immunwork is a biotechnology company specializing in the development of novel drugs for various medical conditions. Their proprietary 'T-E' technology platform is used to create drug molecules with targeting and effector functions, aimed at improving efficacy and reducing toxicity. The company's main offerings include antibody-drug conjugates, antibody-radionuclide conjugates, and ultra-long-acting therapeutic peptides, primarily for the treatment of cancer and other severe clinical conditions. It was founded in 2014 and is based in Taipei City, Taiwan.

O
Orizuru Therapeutics

Orizuru Therapeutics is a company that focuses on the development of regenerative medicine, specifically within the biotechnology and pharmaceutical industry. The company's main service involves the use of induced pluripotent stem cell (iPSC) technology to develop treatments and therapies that can regenerate damaged or diseased tissues. The primary market for Orizuru Therapeutics' offerings is the healthcare sector, particularly areas involved in advanced medical treatments and therapies. It was founded in 2021 and is based in Kyoto, Japan.

B
Biomia

Biomia is a synthetic biology company operating in the healthcare and biotechnology sectors. The company focuses on developing plant-inspired medicines to address unmet medical needs in areas such as pain, addiction, and depression. Its main offerings include the discovery and development of therapeutics for patients suffering from various mental illnesses, and the development of technology to supply these bioactives using fermentation. The company was founded in 2022 and is based in Kgs. Lyngby, Denmark.

Loading...

CBI websites generally use certain cookies to enable better interactions with our sites and services. Use of these cookies, which may be stored on your device, permits us to improve and customize your experience. You can read more about your cookie choices at our privacy policy here. By continuing to use this site you are consenting to these choices.