Refining Therapy for AL
AL Amyloidosis
Amyloidosis
Vaishali Sanchorawala, MD
12th
12 International Myeloma
Myeloma Workshop
Workshop
Washington DC
February 28, 2009

Faculty Disclosure Information
Consultant: No
Grant/Research Support:
pp
Celgene,
g
Johnson & Johnson
Speakers Bureau:
Bureau: Ortho Biotech
Biotech
Major Stock Shareholder: No

Treatment Targets
Tr
T eatment Target
Target
Tr
T eatment
Tr
T eatment Status
Approach
Precursor Protein Production
Chemotherapy
In use: AL
NSAID
In use: AA
Liver Transplant
In use: ATTR
Renal Tr
T ansplant In use: DRA
Fibril Formation
GAG mimetics
Human studies: AA
TTR stabilizers
Human studies: ATTR
Amyloid Deposits
GAG mimetics
Human studies: AA
IDOX
Human studies: AL
SAP depletion
Human studies:
studies: AL

Monitoring Therapeutic Effect
· Key elements
elements
­ Early diagnosis and correct typing
­ Fine balance of chosen treatment regimen and patient's
ability to bear toxicities
· Hematologic complete response
­ Absence of
of monoclonal
monoclonal gammopathy in serum and urine by
by
IFEs
­ Absence of clonal plasma cells in bone marrow biopsy
­ Normalization of
of free
free light chain ratio
ratio
· Organ/Clinical response
­ May take from 3-12 months after treatment
Gertz et al. Am J Hematol, 2005

Conventional Treatment
· Randomized clinical trials of oral cyclic
melphalan and prednisone
­Boston
1
1996
­ Mayo Clinic
2
1997
· Median survival 16 -18 months
· Hematologic complete response rare
· Reversal of organ dysfunction rare
Skinner et al. Am J Med, 1996
Kyle et al. N Eng J Med, 1997

High-
High Dose Melphalan and Stem Cell
Transplantation (HDM/SCT)
· Development of this treatment approach
prompted by promising results of similar
regimens in myeloma.
· Objectives of early clinical trials:
­ Determine
tolerability of this treatment approach in
patients with AL Amyloidosis.
­ Determine
efficacy of this treatment in inducing
complete hematologic response
response.
­ Determine whether complete hematologic
response leads to reversal of amyloid-related
disease and increase
survival.

Prolonged Survival with HDM/SCT
1994-2008
(n=497)
100
Median Survival 73 months
5 year Survival 55%
80
(%)
60
vival
40
Sur
20
0 02468
1
3
5
7
9
10 11
12
13 14
Time (years)
Pt
Pa iti t
en s, n: 497 378 309 256 212 183 151 116
11
83
60
43
24
17
6
3
Sanchorawala et al, ASH 2008

Long-
Long term Outcome after
after HDM/SCT
1994-1997
(n=80)
1.0
n
Md
Me i
dian > 10
0.8
10 yrs
0.6
CR
istributio
estimate
d
0.4
Median 4.1 yrs
p < 0.001
urvival
function 0.2
S
Non-CR
S
0 0
50
100
150
Months
Sanchorawala et al. Blood, 2007

Oral Cyclic Melphalan and
Dexamethasone
N
li ibl f
HDM/SCT
10
· Not eligible for HDM/SCT
1.0
· Hematologic response
0.8
67%, CR 33%
portion
g
· Clinical response 48%
0.6
pro
· Median time to response
0.4
survivin
4 5
. months
months (range 2 3
lativeu
.3-
0.2
10.1)
Cum
· Durable responses
0 0 12 3 47
5
6
· Overall median survival
Survival time, years
5.1 years
Overall survival of 46 AL amyloidosis patients treated
with M-Dex. The median survival is 5.1 years, and the
· TRM 4%
median follow-up of living patients is 5 years (range,
TRM 4%
3.5-6.7 years)
Palladini et al. Blood, 2004
Palladini et al. Blood, 2007

Randomized Study: IFM
100
90
80
al(%)
Melphalan plus dexamethasone
70
a
60
50
40
p = 0.04
llsurviv
30
High-dose melphalan plus stem-cell rescue
Overa
20
10
0 010
20
30
40
50
60
70
80
Months since randomization
Jaccard et al. NEJM, 2007

Comparison of results of HDM/SCT,
Jan 2000-2005 Multi-center vs. Single center
French
BUMC
Intergroup
Number of pts offered
offered SCT
SCT
50
172
Number of pts receiving
37 (74%)
152 (88%)
SCT
Treatment-related mortality
26%
9%
Md
Me i
dian
i
surv val
22.2 month
ths
Nt
Not
h
reac
d
e ,
6 yr survival
52%
Md
Me i
dian f l
o lllow-up
24 months
38 months

What is the Optimal Melphalan-Based
Chemotherapy?
·
HDM/SCT
yields a high rate of complete, durable
hematologic responses, accompanied by clinical
responses
­
High risk of organ-related complications
­
Multidisciplinary patient evaluation and center experience
reduces treatment-related complications
·
Oral melphalan + dexamethasone
also produces
ht
hemat l
o
i
og c
d
an clili i
n
l
ca responses
­
Toxicity due to chronic steroids and alkylating agents
­
Median time to response 4.5 months
·
Further phase III trials in tertiary referral centers are
required
­
MD vs risk adapted HDM/SCT
­
Consider addition of novel agents to the arms

Novel Therapies for AL
AL Amyloidosis
Amyloidosis
· Thalidomide
­ Thalidomide studied as single agent or in combination with
Dexamethasone
­ Single agent
gg
responses,
p
~25%
­ With Dexamethasone, ~50%
­ Thal/Dex combination
· Hematologic response 48%, CR 19%
· Clinical response 26%
­ Poorly tolerated
· 50% Gr 3/4 toxicity as single agent, 65% combined with
Dt
Dexame h
thasone
· Drug withdrawal in 25-50% patients
Seldin et al. Clin Lymphoma, 2003
Dispenzieri et al. Amyloid, 2003
Palladini et al. Blood, 2005

Novel Therapies for AL Amyloidosis
· Lenalidomide
­ Phase II trials at Mayo
y Clinic and Boston
University Medical Center
­ Lenalidomide +/- Dexamethasone
­ Pl
Pre ili i
m nary
l
resu ts i d
n i
dicate better l
to
b
era ili
bility
· Fatigue, rash, leukopenia, thromboses
­ Overall Hematologic
Hematologic Response Rate
Rate
· 56%, CR 27%
­ Median Time to Response
· 6 months (range 3-9)
­ 50% responses durable even after stopping
treatment
Sanchorawala et al, Blood 2007; Dispenzieri et al, Blood
2007; Seldin et al, ASH 2007

Novel Therapies for AL Amyloidosis
py
· Bortezomib
­ International phase I/II trial opened 08/05, completed
accrual
­ Phase I dose-escalation study aimed to determine
MTD f
o once-weekly
d
an t i
w ce-weekl
kly schdl
hedule
d
an
preliminary hematologic response
­ 31 patients with relapsed AL enrolled
­ DLT ­ grade 3 CHF: 2 patients
­ MTD ­ not defined, 1.6 mg/m
2 (once-weekly) and 1.3
mg/m
2
mg/m (twice weekly)
-
used
used for
for phase IIII evaluation
evaluation
­ Hematologic responses 50%, CR 20%
­ Median time to response 1.2 months
Kastritis et al. Haematologica, 2007; Wechalekar et al.
Haematologica, 2008; Reece et al. Blood 2009 (accepted)

Combination Therapies for AL
AL
Amyloidosis
· CTD:
Cyclophosphamide, Thalidomide and
Dexamethasone
­ Hematologic response 74%, CR 21%
­ Md
Me i
dian overallll
i
surv
l
va 41
41 month
ths
­TRM 4%
· MRD:
Melphalan, Lenalidomide and Dexamethasone -
Boston
· CRD:
Cyclophosphamide, Lenalidomide and
Dexamethasone ­ Mayo Clinic
· VMD:
Bortezomib, Melphalan
,p
and Dexamethasone ­ Multi
center trial, poster by Zonder et al
· Vel-Mel transplant:
Bortezomib and melphalan
conditioning for autoSCT, Boston
Wechalekar et al. Blood 2007

Treatment for amyloidosis is increasingly
based on an understanding of the
pathophysiology of the disease

Future Directions
· Clonal plasma cell expansion
­ Anti-plasma cell chemotherapy (current approach)
· Light chain synthesis and secretion
­ Anti-sense and siRNA strategies (Tennesse, Boston)
­ Light chain or oligome
gg
r-mediated cell toxicity
­ LCs or small oligomers may be taken up by cells and mediate acute
organ toxicity
­ Clinical observations
­ In vitro studies: Liao (heart), Trinkaus-Randall (fibroblasts),
Herrera (kidney)
­ Can drugs that block uptake or protect cells from damage be
fd
foun ?
d?
­ Aggregation and fibril formation
­ Very challenging since each LC protein sequence and structure is
different

www.bu.edu/amyloid

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