8-K

As filed with the Securities and Exchange Commission on November 19, 2001

SECURITIES AND EXCHANGE COMMISSION

WASHINGTON, D.C. 20549

FORM 8-K

CURRENT REPORT
Pursuant to Section 13 or 15(d) of the
Securities and Exchange Act of 1934

Date of Report (Date of earliest event reported): November 12, 2001

CV THERAPEUTICS, INC.

(Exact name of Registrant as specified in its charter)

Delaware
(State or other jurisdiction of incorporation or organization) 0-21643
(Commission File No.) 45-1570294
(I.R.S. Employer Identification No.)

3172 Porter Drive
Palo Alto, California 94304
(Address of Principal Executive Offices including Zip Code)

(650) 812-0585
(Registrant’s Telephone Number, Including Area Code)

TABLE OF CONTENTS

	ITEM 5. OTHER EVENTS
	ITEM 7. FINANCIAL STATEMENTS, PRO FORMA FINANCIAL INFORMATION AND EXHIBITS
SIGNATURES
EXHIBIT INDEX
EXHIBIT 99.1
EXHIBIT 99.2
EXHIBIT 99.3

ITEM 5. OTHER EVENTS

     On November 14, 2001, the Registrant publicly disseminated a press release announcing that its Phase III CARISA (Combination Assessment of Ranolazine In Stable Angina ) trial of ranolazine met its primary efficacy endpoint. With patients on a background anti-anginal therapy, ranolazine statistically significantly (p=0.012) increased patients’ symptom-limited exercise duration at trough drug concentrations compared to placebo. Ranolazine represents one of a new class of drugs called pFOX inhibitors for the potential treatment of chronic angina, the attacks of cardiac pain that afflict more than six million people in the United States. The Registrant presented the CARISA results on November 14, 2001 at the late breaking clinical trials session of American Heart Association’s Scientific Sessions 2001.

     On November 12, 2001, the Registrant publicly disseminated a press release announcing the presentation at the 2001 Scientific Sessions of the American Heart Association of results from a retrospective analysis comparing the pro-arrhythmic effects of adenosine and CVT-510, a selective A(1) adenosine receptor agonist, which indicate that after termination of paroxysmal supraventricular tachycardia, a type of atrial arrhythmia, with either adenosine or CVT-510, the use of CVT-510 was associated with fewer abnormal ventricular beats and fewer post-arrhythmia pauses, or skipped heartbeats.

     On November 19, 2001, the Registrant publicly disseminated a press release announcing that in an open-label, dose-ranging Phase II clinical trial in patients with atrial fibrillation or flutter, CVT-510 consistently reduced heart rate from baseline (p<0.05) without decreasing blood pressure. As a result, the Registrant is embarking on a broad Phase IIb development program aimed at defining an optimized dosage regimen in patients with this complex cardiac disease.

     The foregoing descriptions are qualified in their entirety by reference to the Registrant’s Press Releases dated November 14, 2001, November 12, 2001 and November 19, 2001, copies of which are attached hereto as Exhibits 99.1, 99.2 and 99.3, respectively.

     This Current Report on Form 8-K contains forward-looking statements that involve risks and uncertainties. These statements relate to future events or the Registrant’s future clinical or product development or financial performance, including statements as to the Registrant’s development programs, commercialization efforts, and potential products, including ranolazine and CVT-510. In some cases, these forward-looking statements can be identified by terminology such as “may”, “will”, “should”, “expects”, “plans”, “anticipates”, “believes”, “estimates”, “predicts”, “potential” or “continue” or the negative of those terms and other comparable terminology. If one or more of these risks or uncertainties materialize, or if any underlying assumptions prove incorrect, the Registrant’s actual results, performance or achievements may vary materially from any future results, performance or achievements expressed or implied by these forward-looking statements. The Registrant’s actual results may differ materially from the results discussed in the forward-looking statements. Factors that might cause such a difference include, but are not limited to, early stage of development, the timing of clinical trials, the dependence on collaborative and licensing agreements, and other risks detailed from time to time in the Registrant’s filings with the Securities and Exchange Commission, including its Annual Report on Form 10-K for the year ended December 31, 2000.

ITEM 7. FINANCIAL STATEMENTS, PRO FORMA FINANCIAL INFORMATION AND EXHIBITS

     (c)  Exhibits.

99.1	Registrant’s Press Release dated November 14, 2001.
99.2	Registrant’s Press Release dated November 12, 2001.
99.3	Registrant’s Press Release dated November 19, 2001.

2

SIGNATURES

     Pursuant to the requirements of the Securities Exchange Act of 1934, the Registrant has duly caused this report to be signed on its behalf by the undersigned thereunto duly authorized.

CV THERAPEUTICS, INC.
By:	/s/ DANIEL K. SPIEGELMAN
	Daniel K. Spiegelman Senior Vice President and Chief Financial Officer (Principal financial and accounting officer)

3

EXHIBIT INDEX

Exhibit
Number	Description
99.1	Registrant’s Press Release dated November 14, 2001.
99.2	Registrant’s Press Release dated November 12, 2001.
99.3	Registrant’s Press Release dated November 19, 2001.

EX-99.1

                                                                    Exhibit 99.1

FOR IMMEDIATE RELEASE

CV THERAPEUTICS, INC.                                     FLEISHMAN-HILLARD
Dan Spiegelman                                            Carol Harrison
Chief Financial Officer                                   (212) 453-2442
(650) 812-9509

Christopher Chai

Treasurer & Senior Director, Investor Relations
(650) 812-9560

                       CV THERAPEUTICS ANNOUNCES PHASE III
                       CARISA TRIAL MEETS PRIMARY ENDPOINT

      RANOLAZINE RESULTS TO BE PRESENTED AT 2001 AMERICAN HEART ASSOCIATION
                      LATE BREAKING CLINICAL TRIAL SESSION

        ANAHEIM, CALIFORNIA, NOVEMBER 14, 2001 -- CV Therapeutics, Inc. (Nasdaq:
CVTX) today announced that its Phase III CARISA trial of ranolazine met its
primary efficacy endpoint. With patients on a background anti-anginal therapy,
ranolazine statistically significantly (p=0.012) increased patients'
symptom-limited exercise duration at trough drug concentrations compared to
placebo. Ranolazine represents one of a new class of drugs called pFOX
inhibitors for the potential treatment of chronic angina, the attacks of cardiac
pain that afflict more than six million people in the United States. pFOX
inhibitors have the potential to be the first new class of anti-anginal drugs in
the United States in more than 20 years. The CARISA results will be presented
today at the late breaking clinical trials session of American Heart
Association's Scientific Sessions 2001.

        "Results from this trial reveal that patients on ranolazine, in
combination with current anti-anginals, had significantly fewer angina episodes
than patients on placebo, a decrease of about 25 percent. In addition,
ranolazine had only minimal effects on the patients' heart rate and blood
pressure," said Bernard R. Chaitman, M.D., Professor of Medicine, Director of
Cardiovascular Research, St. Louis University School of Medicine, St. Louis,
Missouri, and principal investigator of the CARISA trial. "These data
demonstrate that ranolazine may be an important addition to the current
treatment arsenal for chronic angina."

        "We are very pleased with the results from the CARISA trial of
ranolazine. This combination study is particularly important because most
patients take anti-anginal drugs in combination," said Louis G. Lange, M.D.,
Ph.D., Chairman and Chief Executive Officer of CV Therapeutics, Inc. "With data
from two successfully completed pivotal Phase III trials, MARISA and CARISA, we
will now focus our efforts on preparing our new drug application which we plan
to file with the FDA in 2002."




STUDY DETAIL

        The CARISA (Combination Assessment of Ranolazine In Stable Angina) study
was a Phase III multi-national, randomized, double-blind, placebo-controlled,
parallel group trial of the safety and efficacy of ranolazine. The clinical
trial randomized 823 patients to assess the anti-anginal effects of 12 weeks of
treatment with ranolazine in chronic angina patients also receiving a background
anti-anginal medication. Patients received one of three background therapies
(atenolol 50 mg, diltiazem CD 180 mg, or amlodipine 5 mg) and were randomized to
twice daily doses of ranolazine 750 mg, ranolazine 1000 mg, or placebo. Exercise
testing was performed at trough plasma concentrations (12 hours after dosing)
after 2, 6, and 12 weeks and at peak plasma concentrations (4 hours after
dosing) after 2 and 12 weeks. The prospectively defined primary efficacy
endpoint was symptom-limited exercise duration at trough for all ranolazine
patients compared to placebo at 12 weeks. The CARISA primary efficacy endpoint
of symptom-limited exercise duration at trough has historically been the primary
endpoint that the FDA reviews when considering anti-anginal therapies.

STUDY RESULTS

        In both ranolazine dose groups combined, symptom-limited exercise
duration at trough plasma concentrations, the primary endpoint of the trial,
increased on ranolazine by an average of 116 seconds, compared to an average
increase of 92 seconds on placebo (p=0.012). The average increases in
symptom-limited exercise duration at trough plasma concentrations on each
ranolazine dose, considered independently, were 115 seconds on 750 mg and 116
seconds on 1000 mg, compared to 92 seconds on placebo (p (less than or equal to)
0.03). The increases in exercise times on ranolazine were not significantly
different among the three background therapies; insignificantly greater
increases were seen over diltiazem and amlodipine than over atenolol.

        Statistically significant effects of ranolazine were also observed in
other secondary efficacy endpoints. Ranolazine at doses of 750 mg and 1000 mg
reduced the frequency of angina by an average of 1.3 and 1.7 attacks per week,
respectively, compared to an average decrease of 0.6 attacks per week on placebo
(p (less than or equal to) 0.01 for each dose versus placebo). Compared to
placebo, ranolazine at doses of 750 mg and 1000 mg increased the average time to
electrocardiographic evidence of ischemia; these increases approached
statistical significance at trough (20 and 21 seconds, respectively; p (less
than or equal to) 0.1) and achieved statistical significance at peak (41 and 35
seconds, respectively; p<0.005). In addition, compared to placebo, ranolazine at
both doses statistically significantly increased the average time to onset of
angina at both peak (38 seconds on each dose; p (less than or equal to) 0.003)
and trough (30 and 26 seconds, respectively; p (less than or equal to) 0.05).

        Compared to placebo, systolic blood pressure after 12 weeks of treatment
decreased, on average, by 2 mm Hg on 750 mg (p=NS) and by 3 mm Hg on 1000 mg
(p=0.02). Average heart rate at the same time point was 1 bpm less on either
dose than on placebo, differences which were not statistically significant.

        Side effects more common during ranolazine treatment than during placebo
treatment included constipation, dizziness, nausea, and asthenia. The adverse
event rate was 26% for placebo, 31% for ranolazine 750 mg, and 33% for
ranolazine 1000 mg. Small (<10 milliseconds, similar to MARISA) but
statistically significant (p (less than or equal to) 0.002) increases in QTc
were observed




compared to placebo. Serious adverse events were observed in 6%, 7%, and 7% of
patients on placebo, ranolazine 750 mg, and ranolazine 1000 mg respectively.

CHRONIC ANGINA

        Chronic angina is marked by repeated and sometimes unpredictable attacks
of cardiac pain. Angina attacks occur when the heart is not receiving all the
oxygen it requires to function effectively. These attacks are typically
triggered by physical exertion or emotional stress. Usually angina is associated
with coronary artery disease, which is characterized by a buildup of fatty
plaques in coronary arteries that reduce the flow of oxygen-rich blood through
the heart. According to the American Heart Association, 6.4 million people in
the United States have angina and 400,000 new cases are diagnosed each year.

MECHANISM OF ACTION

        Ranolazine represents one of a new class of compounds called partial
Fatty Acid Oxidation (pFOX) inhibitors, which has the potential to be the first
new anti-anginal drug class in the United States in more than two decades.
Animal studies indicate that pFOX inhibitors increase the efficiency of oxygen
use by the heart, by shifting the heart's metabolism to a fuel source which
requires less oxygen to generate the same amount of energy. The heart uses two
fuels to make energy: fatty acids and glucose (sugar). A healthy heart uses
fatty acids during times of stress. But a heart that is not receiving enough
oxygen-rich blood, due to obstructions in the arteries, can produce more energy
per unit of oxygen consumed using glucose compared to fatty acids. pFOX
inhibitors shift the metabolism of the heart to use more glucose than fatty
acids during stress that might otherwise provoke angina.

RESULTS FROM PRIOR PIVOTAL PHASE III TRIAL

        The CARISA data are similar to and consistent with the results of the
Company's prior Phase III trial of ranolazine, MARISA (Monotherapy Assessment of
Ranolazine In Stable Angina). That trial was a randomized, double-blind,
placebo-controlled trial of ranolazine in patients not receiving any other
anti-anginal drugs. The primary endpoint for MARISA was symptom-limited exercise
duration at the time of trough plasma levels, which was also the primary
endpoint for CARISA.

CONFERENCE CALL

        CV Therapeutics' management will host a conference call on Wednesday,
November 14, 2001, at 2:00 p.m. EST, 11:00 a.m. PST, to discuss the CARISA trial
results. To participate in the conference call, please dial (973) 872-3100. A
replay of the conference call will be available through Friday, November 16,
2001. Domestic and international callers can access the replay by dialing (973)
341-3080; the PIN access number is 2949573.

        Ranolazine has not been approved for marketing by the Food and Drug
Administration or other foreign agencies. Ranolazine is presently being
investigated in clinical trials subject to a United States IND and applicable
foreign authority submissions. CV Therapeutics has not yet submitted an NDA to
the FDA or equivalent application to any other foreign regulatory




authorities for ranolazine, and ranolazine has not yet been determined to be
safe or effective in humans for its intended use.

        CV Therapeutics, Inc., headquartered in Palo Alto, CA, is a
biopharmaceutical company focused on applying molecular cardiology to the
discovery, development and commercialization of novel, small molecule drugs for
the treatment of cardiovascular diseases. CVT currently has four compounds in
clinical trials. Ranolazine, in a new class of compounds known as partial fatty
acid oxidation (pFOX) inhibitors, is being developed for the potential treatment
of chronic angina. CVT-510, an A(1) adenosine receptor agonist, is being
developed for the potential reduction of rapid heart rate during atrial
arrhythmias. CVT-3146, an A(2A) adenosine receptor agonist, is being developed
for the potential use as an adjunctive pharmacologic agent in cardiac perfusion
imaging studies. Adentri(TM), an A(1) adenosine antagonist, is being developed
by our partner Biogen, Inc., for the potential treatment of acute and chronic
congestive heart failure. For more information, please visit CV Therapeutics'
website at http://www.cvt.com.

        Except for the historical information contained herein, the matters set
forth in this press release, including statements as to the company's
development programs, commercialization efforts, and potential products,
including ranolazine, are forward-looking statements within the meaning of the
"safe harbor" provisions of the Private Securities Litigation Reform Act of
1995. These forward-looking statements are subject to risks and uncertainties
that may cause actual results to differ materially, including, early stage of
development; the timing of clinical trials; the dependence on collaborative and
licensing agreements; and other risks detailed from time to time in CVT's SEC
reports, including its Annual Report on Form 10-K for the year ended December
31, 2000. CVT disclaims any intent or obligation to update these forward-looking
statements.

                                       ###

EX-99.2

                                                                    Exhibit 99.2

FOR IMMEDIATE RELEASE

CV THERAPEUTICS, INC.                                     FLEISHMAN-HILLARD
Dan Spiegelman                                            Carol Harrison
SVP & Chief Financial Officer                             (212) 453-2442
(650) 812-9509

Christopher Chai
Treasurer & Senior Director, Investor Relations
(650) 812-9560

            CV THERAPEUTICS ANNOUNCED THAT CVT-510 MAY TERMINATE PSVT
              WITH FEWER PROARRHYTHMIC SIDE EFFECTS THAN ADENOSINE

Data Presented at the 2001 Scientific Sessions at the American Heart Association

        ANAHEIM, CALIFORNIA, NOVEMBER 12, 2001 -- CV Therapeutics, Inc. (Nasdaq:
CVTX) today announced the presentation of results from a retrospective analysis
comparing the pro-arrhythmic effects of adenosine and CVT-510, a selective A(1)
adenosine receptor agonist. Data from this analysis indicated that after
termination of paroxysmal supraventricular tachycardia (PSVT), a type of atrial
arrhythmia, with either adenosine or CVT-510, the use of CVT-510 was associated
with fewer abnormal ventricular beats and fewer post-arrhythmia pauses, or
skipped heartbeats. These data were presented at the 2001 Scientific Sessions of
the American Heart Association. Current clinical trials for CVT-510 include a
Phase III trial in patients with PSVT and a Phase II trial in patients with
atrial fibrillation.

        "Data from this analysis suggest that a selective A(1) adenosine
agonist, like CVT-510, may convert PSVT to normal sinus rhythm with fewer
pro-arrhythmic side effects than adenosine, enabling the patients to experience
a smooth termination of their arrhythmia. These results warrant further
investigation in a controlled clinical study," said Imran Niazi, M.D., Director
of the Wisconsin Center of Clinical Research, and lead author of this study.

        Data for this retrospective analysis were compiled from a previously
reported clinical trial which was conducted to evaluate the effect of CVT-510 in
terminating PSVT induced in an electrophysiology lab. Data from 14 patients who
converted to sinus rhythm after receiving CVT-510 at two study centers and from
12 patients who converted to sinus rhythm after receiving adenosine at one of
the study centers during a similar time period, were included in the analysis.
Both patient groups had similar demographics and a similar mechanism of PSVT. In
a comparison of the data from these two groups, there were statistically
significantly fewer patients with abnormal ventricular beats or post-arrhythmia
pauses in the CVT-510 group as compared with the adenosine group. Additionally,
the longest post-arrhythmia pause in the CVT-510 patient group was 1.5 seconds
whereas the longest pause in the adenosine group was 7.3 seconds. Many patients
with atrial arrhythmias are elderly and have pre-existing diseases involving the




electrical conduction system of the heart. An agent that is associated with
shorter pauses and fewer abnormal ventricular beats may offer an advantage.

        Over 2.6 million times per year, patients are admitted to U.S. hospitals
and emergency rooms with a primary or secondary diagnosis of atrial arrhythmias.
Atrial arrhythmias, such as atrial fibrillation, atrial flutter and PSVT, can
cause potentially life-threatening low blood pressure, and may also result in
stroke or heart attack.

        Atrial arrhythmias occur when electrical signals in the atria cause the
heart to beat too rapidly or uncontrollably. The AV node controls the
transmission of electrical impulses from the atria to the ventricles. When the
frequency of signals passing through the AV node is too high, the ventricles, in
turn, begin to beat too rapidly. This results in insufficient time for filling
and emptying the left ventricle, which causes low blood pressure (hypotension)
and reduced blood flow to the brain and other vital organs. Therefore, the heart
rate needs to be controlled urgently.

        Clinical studies conducted with intravenous CVT-510 suggest that it may
slow the speed of AV nodal conduction by selectively stimulating the A(1)
adenosine receptor, and could avoid blood pressure lowering because it does not
stimulate the A(2) adenosine receptor. Thus, it may be possible to use
intravenous CVT-510 for rapid intervention in the control of atrial arrhythmias
without lowering blood pressure.

        CV Therapeutics, Inc., headquartered in Palo Alto, CA, is a
biopharmaceutical company focused on applying molecular cardiology to the
discovery, development and commercialization of novel, small molecule drugs for
the treatment of cardiovascular diseases. CVT currently has four compounds in
clinical trials. Ranolazine, the first in a new class of compounds known as
partial fatty acid oxidation (pFOX) inhibitors, is being developed for the
potential treatment of chronic angina. CVT-510, an A(1) adenosine receptor
agonist, is being developed for the potential reduction of rapid heart rate
during atrial arrhythmias. CVT-3146, an A(2A) adenosine receptor agonist, is
being developed for the potential use as an adjunctive pharmacologic agent in
cardiac perfusion imaging studies. Adentri(TM), an A(1) adenosine antagonist, is
being developed by our partner Biogen, Inc., for the potential treatment of
acute and chronic congestive heart failure. For more information, please visit
CV Therapeutics' website at http://www.cvt.com.

        Except for the historical information contained herein, the matters set
forth in this press release, including statements as to the company's
development programs, commercialization efforts, and potential products,
including CVT-510, are forward-looking statements within the meaning of the
"safe harbor" provisions of the Private Securities Litigation Reform Act of
1995. These forward-looking statements are subject to risks and uncertainties
that may cause actual results to differ materially, including, early stage of
development; the timing of clinical trials; the dependence on collaborative and
licensing agreements; and other risks detailed from time to time in CVT's SEC
reports, including its Annual Report on Form 10-K for the year ended December
31, 2000. CVT disclaims any intent or obligation to update these forward-looking
statements.

                                                 ###

EX-99.3

                                                                    Exhibit 99.3


FOR IMMEDIATE RELEASE

CV THERAPEUTICS, INC.                                       FLEISHMAN-HILLARD
Dan Spiegelman                                              Carol Harrison
Chief Financial Officer                                     (212) 453-2442
(650) 812-9509

Christopher Chai
Treasurer & Senior Director, Investor Relations
(650) 812-9560


                  CV THERAPEUTICS DEMONSTRATES PROOF OF CONCEPT
           FOR CVT-510 IN PHASE II ATRIAL FIBRILLATION CLINICAL TRIAL

         PALO ALTO, CALIFORNIA, NOVEMBER 19, 2001 - CV Therapeutics, Inc.
(Nasdaq: CVTX) announced today that in an open-label, dose-ranging Phase II
clinical trial in patients with atrial fibrillation or flutter, CVT-510
consistently reduced heart rate from baseline (p<0.05) without decreasing blood
pressure. The Company is therefore embarking on a broad Phase IIb development
program aimed at defining an optimized dosage regimen in patients with this
complex cardiac disease. Current clinical trials for CVT-510 include a Phase III
trial in patients with PSVT and Phase II trials in patients with atrial
fibrillation.

          "We are pleased that the CVT-510 program has successfully established
proof of concept for reduction of heart rate in atrial fibrillation, and is now
committed to a broader Phase IIb program," said Louis G. Lange, M.D., Ph.D.,
Chairman and Chief Executive Officer of CV Therapeutics, Inc. "With our strong
balance sheet of approximately $350 million in cash, we can continue to move our
clinical programs forward."

         Over 2.6 million times per year, patients are admitted to U.S.
hospitals and emergency rooms with a primary or secondary diagnosis of atrial
arrhythmias. Atrial arrhythmias, such as atrial fibrillation, atrial flutter and
paroxysmal supraventricular tachycardia (PSVT), can cause potentially
life-threatening low blood pressure, and may also result in stroke or heart
attack.

         Atrial arrhythmias occur when electrical signals in the atria cause the
heart to beat too rapidly or uncontrollably. The AV node controls the
transmission of electrical impulses from the atria to the ventricles. When the
frequency of signals passing through the AV node is too high, the ventricles, in
turn, begin to beat too rapidly. This results in insufficient time for filling
and emptying the left ventricle, which causes low blood pressure (hypotension)
and reduced blood flow to the brain and other vital organs. Therefore, the heart
rate needs to be controlled urgently.

         Clinical studies conducted with intravenous CVT-510 suggest that it may
slow the speed of AV nodal conduction by selectively stimulating the A(1)
adenosine receptor, and could avoid blood pressure lowering because it does not
stimulate the A(2) adenosine receptor. Thus, it may be

possible to use intravenous CVT-510 for rapid intervention in the control of
atrial arrhythmias without lowering blood pressure.

         CV Therapeutics, Inc., headquartered in Palo Alto, CA, is a
biopharmaceutical company focused on applying molecular cardiology to the
discovery, development and commercialization of novel, small molecule drugs for
the treatment of cardiovascular diseases. CVT currently has four compounds in
clinical trials. Ranolazine, in a new class of compounds known as partial fatty
acid oxidation (pFOX) inhibitors, is being developed for the potential treatment
of chronic angina. CVT-510, an A(1) adenosine receptor agonist, is being
developed for the potential reduction of rapid heart rate during atrial
arrhythmias. CVT-3146, an A(2)A adenosine receptor agonist, is being developed
for the potential use as an adjunctive pharmacologic agent in cardiac perfusion
imaging studies. Adentri(TM), an A(1) adenosine antagonist, is being developed
by our partner Biogen, Inc., for the potential treatment of acute and chronic
congestive heart failure. For more information, please visit CV Therapeutics'
website at http://www.cvt.com.

         Except for the historical information contained herein, the matters set
forth in this press release, including statements as to the company's
development programs, commercialization efforts, and potential products,
including CVT-510, are forward-looking statements within the meaning of the
"safe harbor" provisions of the Private Securities Litigation Reform Act of
1995. These forward-looking statements are subject to risks and uncertainties
that may cause actual results to differ materially, including, early stage of
development; the timing of clinical trials; the dependence on collaborative and
licensing agreements; and other risks detailed from time to time in CVT's SEC
reports, including its Annual Report on Form 10-K for the year ended December
31, 2000. CVT disclaims any intent or obligation to update these forward-looking
statements.

                                       ###