RATIONALE: SU5416 may stop the growth of cancer by stopping blood flow to the tumor. Androgens can stimulate the growth of prostate cancer cells. Hormone therapy using flutamide, bicalutamide, leuprolide, or goserelin may fight prostate cancer by reducing the production of androgens. Radiation therapy uses high-energy x-rays to damage tumor cells. Combining SU5416, hormone therapy, and radiation therapy may kill more tumor cells.
PURPOSE: Phase I trial to study the effectiveness of SU5416 plus hormone therapy and radiation therapy in treating patients who have prostate cancer.

Start Date01 Nov 2001

Sponsor / Collaborator

The University of Chicago

[+1]

NCT00023738

/ CompletedPhase 1/2IIT

A Phase I/II Study Of Neoadjuvant Chemotherapy, Angiogenesis Inhibitor SU5416 (NSC # 696819; A TK Inhibitor Anti-Angionesises Compound), And Radiation Therapy In The Management Of High Risk, High-Grade, Soft Tissue Sarcomas Of The Extremities And Body Wall

RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Drugs such as SU5416 may stop the growth of cancer by stopping blood flow to the tumor. Radiation therapy uses high-energy x-rays to damage tumor cells. Giving chemotherapy, SU5416, and radiation therapy before and after surgery may kill more tumor cells.
PURPOSE: Phase I/II trial to study the effectiveness of chemotherapy, SU5416, radiation therapy, and surgery in treating patients who have soft tissue sarcoma.

Start Date01 Aug 2001

Sponsor / Collaborator

Radiation Therapy Oncology Group

[+1]

NCT00023725

/ CompletedPhase 1/2IIT

A Randomized Phase I/II Study Of Preoperative Radiotherapy With/Without SUGEN 5416 (NSC # 696819; A TK Inhibitor Anti-Angiogenesis Compound) In The Management Of Low To Intermediate Grade Soft Tissue Sarcoma Of The Trunk or Extremity

RATIONALE: Radiation therapy uses high-energy x-rays to damage tumor cells. Drugs such as SU5416 may stop the growth of cancer by stopping blood flow to the tumor. It is not yet known if radiation therapy is more effective with or without SU5416 in treating soft tissue sarcoma.
PURPOSE: Phase I/II trial to compare the effectiveness of radiation therapy with or without SU5416 in treating patients who have stage IB or stage IIA soft tissue sarcoma.

Start Date01 Aug 2001

Sponsor / Collaborator

Radiation Therapy Oncology Group

[+1]

100 Clinical Results associated with Semaxanib

100 Translational Medicine associated with Semaxanib

100 Patents (Medical) associated with Semaxanib

860

Literatures (Medical) associated with Semaxanib

31 Dec 2025·CLINICAL AND EXPERIMENTAL HYPERTENSION

Cinnamaldehyde alleviates pulmonary hypertension by affecting vascular remodeling through the TLR4/NF-kB/HIF-1a pathway

Article

Author: Zhang, Jinbo ; Tian, Zhengkun ; Yang, Zhiyong ; Wang, Chunhe ; Fan, Bingbing ; Zhang, Wenxin

OBJECTIVE:

To investigate the mechanism by which cinnamaldehyde (CA) alleviates pulmonary arterial hypertension (PAH) through the TLR4/NF-kB/HIF-1a pathway.

METHODS:

PAH was induced in rats via SU5416 injection and hypoxia. Hemodynamics (RVMP, RVSP, mPAP) were measured. Histological changes were assessed by HE staining, and protein expressions of α-SMA, Col I, TLR4, p-p65, p65, and HIF-1a were detected by western blot. In vitro, hypoxia-induced HPAECs were treated with CA and TLR4 activator RS09TFA. Cell function was assessed by CCK-8, colony formation, and scratch assays, with VE-Cadherin and α-SMA expression analyzed by western blot.

RESULTS:

PAH rats showed increased RVMP, RVSP, mPAP, and pulmonary artery thickening. CA significantly alleviated lung damage and reduced α-SMA and Col I expression. TLR4/NF-kB/HIF-1a activation with RS09TFA inhibited CA's effects. In vitro, CA mitigated hypoxia-induced HPAEC dysfunction, restoring VE-Cadherin and α-SMA expression, while RS09TFA blocked these effects.

CONCLUSION:

CA alleviates PAH by inhibiting the TLR4/NF-kB/HIF-1a pathway and suppressing vascular remodeling, suggesting its potential as a therapeutic agent for PAH.

01 Jun 2025·BIOCHEMICAL PHARMACOLOGY

xCT/Slc7a11 promotes pulmonary arterial hypertension by disrupting AMPKα suppression of mTOR activation

Article

Author: Qi, Xianmei ; Liu, Jie ; Chen, Hongyu ; Zhang, Hongbing ; Zheng, Cuiting ; Gao, Zhenqiang ; Meng, Yan ; Zhang, Xiyu ; Liu, Fangming ; Wang, Chen ; Chen, Chen ; Li, Kai ; Wu, Yuting ; Zhao, Heng ; Deng, Weiwei

While mTOR plays a key role in the development of pulmonary arterial hypertension (PAH), its suppressor, AMPKα, acts as an inhibitor. Although mTOR-driven transcriptional upregulation of the plasma membrane exchanger and amino acid transporter xCT, encoded by the Slc7a11 gene, is critical for cell proliferation and tumorigenesis, the involvement of xCT in PAH remains unexplored. In this study, we found that xCT expression was elevated in hypoxia-treated human pulmonary arterial endothelial cells (HPAECs) and the lungs of hypoxia-exposed mice and Sugen5416/hypoxia (SuHx)-induced PAH mice. Knockout of xCT prevented the development of PAH and right heart failure in SuHx-conditioned mice. The xCT inhibitor sulfasalazine prevented and reversed SuHx-induced PAH in mice. Deleting and inhibiting xCT activated AMPKα and inactivated mTOR in mouse lungs with PAH and in HPAECs. Sulfasalazine suppressed mTOR through activation of AMPKα in HPAECs. The mTOR inhibitor rapamycin reduced xCT expression, activated AMPKα, and suppressed mTOR in HPAECs. These findings suggest that xCT promotes the development of PAH, likely through suppression of AMPKα and activation of mTOR. Blockage of xCT and mTOR or activation of AMPKα by existing drugs such as sulfasalazine, sirolimus, and metformin may offer readily therapeutic strategies for PAH.

01 Jun 2025·British Journal of Pharmacology

Imatinib aggravates pressure‐overload‐induced right ventricle failure via JNK/Runx2 pathway

Article

Author: Zhou, Liang ; Wu, Zhixiong ; Wang, Tao ; Lu, Wenju ; Chen, Lingdan ; Ding, Shangwei ; Ma, Zhuoji ; Bai, Qianwen ; Chen, Xin ; Zeng, Xiaohui ; Wang, Jian ; Cen, Chunxian ; Hong, Wanxian ; Wen, Shanshan

Abstract:

Background and Purpose:

Right ventricular (RV) function is the key prognostic determinant of pulmonary hypertension (PH). In PH patients, imatinib treatment decreases pulmonary vascular resistance and improves exercise capacity, but does not change mortality or duration to clinical worsening. Imatinib has been reported to be cardiotoxic in the left heart. We hypothesise that imatinib damages the pressure overloaded RV via its direct effects within the heart, which may counteract its therapeutic effects in haemodynamic improvement of PH.

Experimental Approach:

A pulmonary arterial banding (PAB) rat model with fixed pulmonary artery narrowing was performed to avoid changes in RV afterload.

Key Results:

In PAB rats, imatinib treatment decreased the survival rate and exacerbated RV dysfunction, myocardial hypertrophy, apoptosis and fibrosis. In vitro, imatinib increased cardiomyocyte hypertrophy and did not change cardiac fibroblasts activation; however, imatinib‐treated conditioned medium from cardiomyocytes promoted fibroblast activation. Mechanistically, imatinib increased the phosphorylation of c‐jun N‐terminal kinase (JNK) and the expression of RUNX family transcription factor 2 (Runx2), and subsequently promoted the transcription of thrombospondin 4 (THBS4) and connective tissue growth factor (CTGF) in RV cardiomyocytes. Finally, SP600125, a JNK inhibitor, significantly alleviated imatinib‐induced RV failure in PAB rats and enhanced the effects of imatinib on RV function improvement in SU5416 + hypoxia‐induced PH rats without affecting pulmonary artery narrowing.

Conclusion and Implications:

We demonstrate for the first time that imatinib aggravates RV failure under pressure overload through JNK/Runx2 pathway, and JNK inhibition improves the therapeutic effects of imatinib on RV function in PH.

News (Medical) associated with Semaxanib

13 Jun 2022

·www.globenewswire.com

Keros Therapeutics Presents Results from a Preclinical Study of RKER-012 in Pulmonary Arterial Hypertension at the Pulmonary Hypertension Association International Conference and Scientific Sessions

LEXINGTON, Mass., June 13, 2022 (GLOBE NEWSWIRE) -- Keros Therapeutics, Inc. (“Keros” or the “Company”) (Nasdaq: KROS), a clinical-stage biopharmaceutical company focused on the discovery, development and commercialization of novel treatments for patients suffering from hematological and musculoskeletal disorders with high unmet medical need, today announced results from a preclinical study of RKER-012 on cardiac and pulmonary pathology in an established rodent model of pulmonary arterial hypertension (“PAH”), which were presented at the Pulmonary Hypertension Association International Conference and Scientific Sessions held on June 10 through 12, 2022. RKER-012 reduced cardiac and pulmonary pathology in a rodent PAH model. RKER-012, a Novel Activin Receptor Type IIB (“ActRIIB”) Ligand Trap, Reduced Cardiac and Pulmonary Pathology in a Sugen/Hypoxia Model of PAH Keros combined administration of SUGEN5416, a tyrosine kinase inhibitor of vascular endothelial growth factor receptors 1/2, with exposure to chronic hypoxia to recapitulate the biology in PAH. A research form of KER-012 (“RKER-012”) was tested in this SUGEN/hypoxia (“SH”) rat model of PAH. Adult male rats were subjected to SH and received either vehicle, 10 mg/kg of activin receptor type IIA-Fc (“ActRIIA-Fc”) or 10 mg/kg RKER-012 twice weekly for three weeks. Rats maintained under normal oxygen conditions (“normoxic controls”) received only vehicle. Consistent with the development of cardiac and pulmonary impairment, vehicle-treated SH rats exhibited increases in Fulton index, which measures enlargement of the right ventricle (p<0.0001) and systolic pulmonary arterial pressure (“sPAP”) (p<0.0001) relative to normoxic controls. Treatment of the SH rats with ActRIIA-Fc did not significantly attenuate increased Fulton index (p>0.05) and sPAP (p>0.05) relative to the vehicle-treated SH rats. However, relative to the vehicle-treated SH rats, treatment of the SH rats with RKER-012 significantly attenuated increased Fulton index (p<0.01) and prevented an increase in sPAP (p<0.001). Additionally, vehicle-treated SH rats exhibited increased lung inflammation/fibrosis (p<0.0001), smooth muscle hypertrophy (p<0.0001), and arteriole muscularization (p<0.0001) relative to normoxic controls, while treatment with RKER-012 reduced these pathologies (all p<0.0001, relative to vehicle). Vehicle-treated SH rats also exhibited increased expression of atrial natriuretic peptide (“ANP”) and brain natriuretic peptide (“BNP”; both p<0.05) relative to normoxic controls. Treatment with RKER-012 significantly reduced ANP expression (p<0.05) and trended to reduce BNP expression (p=0.11), which Keros believes indicates that RKER-012 could potentially reduce PAH-induced damage to the heart. Vehicle-treated SH rats also exhibited elevated expression of genes associated with the development of PAH-associated pathology in the lung and right ventricle, both hallmarks of PAH pathology, which were reduced with RKER-012 treatment. In a study evaluating the binding activity of KER-012, KER-012 was observed to inhibit ligands associated with endothelial dysfunction, including activins A and B, and had a reduced affinity for BMP-9 compared to activin receptor type IIA. Finally, in an in vitro study, human pulmonary arterial endothelial cells (“HPAECs”) were treated with RKER-012 (10 µg/mL) and placed into either normoxic or hypoxic conditions. HPAECs exposed to hypoxic conditions for 48 hours had significantly elevated expression of activin A (p<0.05) and increased levels of free activin A (p<0.01) relative to cells in normoxic conditions. Treatment with RKER-012 reversed the observed hypoxia-mediated increases in activin expression. Taken together, Keros believes these data provide early evidence that KER-012 has the potential to benefit the vasculature, lung and heart tissues in patients with PAH. About KER-012 KER-012 is designed to bind to and inhibit the signaling of TGF-ß ligands that suppress bone growth, including activin A and activin B. Keros believes that KER-012 has the potential to increase the signaling of bone morphogenic protein (“BMP”) pathways through this inhibition of activin A and activin B signaling, and consequently treat diseases such as PAH that are associated with reduced BMP signaling due to inactivating mutations in the BMP receptors. KER-012 is being developed for the treatment of PAH and for the treatment of disorders associated with bone loss, such as osteogenesis imperfecta and osteoporosis. About Keros Therapeutics, Inc. Keros is a clinical-stage biopharmaceutical company focused on the discovery, development and commercialization of novel treatments for patients suffering from hematologic and musculoskeletal disorders with high unmet medical need. Keros is a leader in understanding the role of the transforming growth factor-beta family of proteins, which are master regulators of red blood cell and platelet production as well as of the growth, repair and maintenance of muscle and bone. Keros’ lead protein therapeutic product candidate, KER-050, is being developed for the treatment of low blood cell counts, or cytopenias, including anemia and thrombocytopenia, in patients with myelodysplastic syndromes and in patients with myelofibrosis. Keros’ lead small molecule product candidate, KER-047, is being developed for the treatment of anemia resulting from iron imbalance. Keros’ third product candidate, KER-012, is being developed for the treatment of PAH and for the treatment of disorders associated with bone loss, such as osteoporosis and osteogenesis imperfecta. Cautionary Note Regarding Forward-Looking Statements Statements contained in this press release regarding matters that are not historical facts are “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995, as amended. Words such as “anticipates,” “believes,” “expects,” “intends,” “plans,” “potential,” “projects,” “would” and “future” or similar expressions are intended to identify forward-looking statements. Examples of these forward-looking statements include statements concerning: the potential of KER-012 to benefit lung and heart tissues in patients with PAH. Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward-looking statements. These risks and uncertainties include, among others: Keros’ limited operating history and historical losses; Keros’ ability to raise additional funding to complete the development and any commercialization of its product candidates; Keros’ dependence on the success of its lead product candidates, KER-050 and KER-047; that Keros may be delayed in initiating, enrolling or completing any clinical trials; competition from third parties that are developing products for similar uses; Keros’ ability to obtain, maintain and protect its intellectual property; Keros’ dependence on third parties in connection with manufacturing, clinical trials and pre-clinical studies; Keros’ ability to enter into new collaborations; and risks relating to the impact on our business of the COVID-19 pandemic or similar public health crises. These and other risks are described more fully in Keros’ filings with the Securities and Exchange Commission (“SEC”), including the “Risk Factors” section of the Company’s Quarterly Report on Form 10-Q, filed with the SEC on May 5, 2022, and its other documents subsequently filed with or furnished to the SEC. All forward-looking statements contained in this press release speak only as of the date on which they were made. Except to the extent required by law, Keros undertakes no obligation to update such statements to reflect events that occur or circumstances that exist after the date on which they were made. Investor Contact: Justin Frantzjfrantz@soleburytrout.com617-221-9100

Small molecular drugCollaborate

14 May 2021

·www.biospace.com

Keros Therapeutics Presents Results from Preclinical Study of KER-012 in Pulmonary Arterial Hypertension at the American Thoracic Society International Conference

LEXINGTON, Mass., May 14, 2021 (GLOBE NEWSWIRE) -- Keros Therapeutics, Inc. (“Keros” or the “Company”) (Nasdaq: KROS), a clinical-stage biopharmaceutical company focused on the discovery, development and commercialization of novel treatments for patients suffering from hematological and musculoskeletal disorders with high unmet medical need, today announced results from a preclinical study of KER-012 on pulmonary and cardiac dysfunction in an established rodent model of pulmonary arterial hypertension (“PAH”) at the virtual American Thoracic Society International Conference held May 14 through 19, 2021. Additional data from a previously conducted nonclinical study in cynomolgus monkeys was also included in the presentation. KER-012 prevented markers of inflammation and fibrosis, and vascular remodeling in a rodent PAH model and did not alter red blood cell number in rats or non-human primates. RKER-012, a Novel Activin Receptor Type IIB (ActRIIB) Ligand Trap, Reduced Cardiopulmonary Pathology in a Rodent Model of Pulmonary Arterial Hypertension Keros combined administration of SUGEN5416, a tyrosine kinase inhibitor of vascular endothelial growth factor receptors 1/2, with exposure to chronic hypoxia to recapitulate the biology in PAH. A research form of KER-012 (“RKER-012”) was tested in this SUGEN/hypoxia (“SH”) rat model of PAH. Adult male rats were subjected to SH and received either vehicle or 10 mg/kg RKER-012 twice weekly for four weeks. Rats maintained under normal oxygen conditions (“normoxic controls”) received only vehicle. Consistent with enhanced pulmonary vascular remodeling and cardiac fibrosis, vehicle-treated SH rats showed significantly greater right ventricle plasminogen activator inhibitor-1 (“PAI-1”) expression (+236.7%; p<0.05), α-smooth muscle actin (“α-SMA”) expression (+255.4%; p<0.05) and increased arterial wall thickness (+43.8%, p<0.001), relative to normoxic controls. Treatment with RKER-012 reduced heart PAI-1 expression and lung α-SMA to levels equivalent to normoxic controls and reduced arterial wall thickness, which Keros believes suggests that KER-012 could potentially prevent the progression of PAH. Additionally, vehicle-treated SH rats had significantly greater neutrophil number (+139.2%; p<0.01) relative to normoxic controls. Treatment with RKER-012 reduced neutrophils to levels of normoxic controls, indicating a reduction in PAH-associated inflammation. There was no effect of SH or RKER-012 on either white blood cells or lymphocytes. Finally, vehicle-treated SH rats had significantly greater Fulton index, which measures enlargement of the right ventricle (+21.7; p<0.0001), as well as trends for increased atrial natriuretic peptide (“ANP”) (+172.8%; p=0.18) and B-type natriuretic peptide (“BNP”) (+38.7%; p=0.057), relative to normoxic controls. Treatment with RKER-012 reduced Fulton Index to control levels, and reduced ANP and BNP expression to levels below controls, which Keros believes indicates that KER-012 could potentially reduce PAH-induced damage to the heart. RKER-012 did not increase red blood cell number in the SH rats, relative to either vehicle-treated SH rats or normoxic controls. Similarly, KER-012 did not increase red blood cells in healthy naïve non-human primates, a model highly translatable to humans. “The Keros team is presenting exciting data on our KER-012 program at ATS. PAH is associated with imbalanced signaling in the transforming growth factor-beta (“TGF-ß”) pathway, and the results of this study suggest that KER-012 prevented disease progression in this PAH model, which we believe supports our hypothesis that rebalancing signaling by inhibiting certain ligands may provide benefit in PAH,” said Jasbir S. Seehra, Ph.D., President and Chief Executive Officer of Keros. “Additionally, treatment with KER-012 did not increase red blood cells in both rats and nonhuman primates, which can result from inhibition of this pathway. We believe that the current study supports that KER-012 has the potential to treat PAH in patients without dose-limiting increases in red blood cells.” About KER-012 KER-012 is designed to bind to and inhibit the signaling of TGF-ß ligands, including activin A and activin B, which are key regulators of bone remodeling that act to suppress bone growth. Keros believes that KER-012 has the potential to increase the signaling of bone morphogenic protein (“BMP”) pathways through this inhibition of activin A and activin B signaling, and consequently treat diseases such as PAH that are associated with reduced BMP signaling due to inactivating mutations in the BMP receptors. KER-012 is being developed for the treatment of disorders associated with bone loss, such as osteogenesis imperfecta and osteoporosis, and for the treatment of PAH. About Keros Therapeutics, Inc. Keros is a clinical-stage biopharmaceutical company focused on the discovery, development and commercialization of novel treatments for patients suffering from hematologic and musculoskeletal disorders with high unmet medical need. Keros is a leader in understanding the role of the Transforming Growth Factor-Beta family of proteins, which are master regulators of red blood cell and platelet production as well as of the growth, repair and maintenance of muscle and bone. Keros’ lead protein therapeutic product candidate, KER-050, is being developed for the treatment of low blood cell counts, or cytopenias, including anemia and thrombocytopenia, in patients with myelodysplastic syndromes and in patients with myelofibrosis. Keros’ lead small molecule product candidate, KER-047, is being developed for the treatment of anemia resulting from iron imbalance, as well as for the treatment of fibrodysplasia ossificans progressiva. Keros’ third product candidate, KER-012, is being developed for the treatment of disorders associated with bone loss, such as osteoporosis and osteogenesis imperfecta, and for the treatment of pulmonary arterial hypertension. Cautionary Note Regarding Forward-Looking Statements Statements contained in this press release regarding matters that are not historical facts are “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995, as amended. Words such as "anticipates," "believes," "expects," "intends," “plans,” “potential,” "projects,” “would” and "future" or similar expressions are intended to identify forward-looking statements. Examples of these forward-looking statements include statements concerning: the potential of KER-012 to treat diseases such as PAH without dose-limiting increases in red blood cells. Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward-looking statements. These risks and uncertainties include, among others: Keros’ limited operating history and historical losses; Keros’ ability to raise additional funding to complete the development and any commercialization of its product candidates; Keros’ dependence on the success of its lead product candidates, KER-050 and KER-047; that Keros may be delayed in initiating, enrolling or completing any clinical trials; competition from third parties that are developing products for similar uses; Keros’ ability to obtain, maintain and protect its intellectual property; Keros’ dependence on third parties in connection with manufacturing, clinical trials and pre-clinical studies; Keros’ ability to enter into new collaborations; and risks relating to the impact on our business of the COVID-19 pandemic or similar public health crises. These and other risks are described more fully in Keros’ filings with the Securities and Exchange Commission (“SEC”), including the “Risk Factors” section of the Company’s Quarterly Report on Form 10-Q, filed with the SEC on May 6, 2021, and its other documents subsequently filed with or furnished to the SEC. All forward-looking statements contained in this press release speak only as of the date on which they were made. Except to the extent required by law, Keros undertakes no obligation to update such statements to reflect events that occur or circumstances that exist after the date on which they were made. Investor Contact: Julia Balanova jbalanova@soleburytrout.com 646-378-2936

Small molecular drugCollaborate

100 Deals associated with Semaxanib

External Link

KEGG	Wiki	ATC	Drug Bank
D05819	Semaxanib	-	DB06436

R&D Status

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Metastatic Colorectal Carcinoma	Phase 3	United States	Pfizer Inc.	01 Nov 1999
Kaposi Sarcoma	Phase 3	United Kingdom	-	-
Non-Small Cell Lung Cancer	Phase 3	United States	-	-
AIDS-related Kaposi Sarcoma	Phase 2	United States	Sugen, Inc.	31 Aug 2001
Acute Myeloid Leukemia	Phase 2	United States	-	-
Acute Myeloid Leukemia	Phase 2	Germany	-	-
Acute Myeloid Leukemia	Phase 2	Switzerland	-	-

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


ATS2024	Not Applicable	Pulmonary Arterial Hypertension	-	SU5416	waccfxhhar(qtgwwtxlji) = jjrxnbiruw apwqfabrfa (pnykjrpfbq )	-	19 May 2024
NCT00006247 (Pubmed \| Pediatr Blood Cancer)	Phase 1	Childhood Central Nervous System Neoplasm	33	SU5416	rcegpzwlzm(hvhhorvuee) = ncqckkdznh mgztedpwjz (ntbiwirldu ) View more	-	01 Feb 2009
ARVO2003	Not Applicable	Retinal Diseases	-	SU5416 25 mg/kg/day	lsbgvfgzen(evxdvgnxxz) = reduced to normoxic control levels with both treatments of SU5416 zywbzjmnkx (lgpwdnrisb )	-	01 May 2003
ARVO2003	Not Applicable	Retinal Diseases	-	SU5416 50 mg/kg/day		-	01 May 2003

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